1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.

1) SUCCIMER: INITIAL DOSE: 10 mg/kg or 350 mg/m(2) every 8 hours orally for 5 days, then increase interval to every 12 hours for next 14 days; repeat course(s) if indicated. A minimum of 2 weeks between courses is recommended, unless the patient's symptoms or blood concentrations indicate a need for more prompt treatment.
2) D-PENICILLAMINE: Use only if less toxic agents not available or not tolerated. USUAL DOSE: ADULT: 1 to 1.5 g/day given orally in 4 divided doses. CHILD: 15 to 30 mg/kg/day in 3 to 4 divided doses. Initially, a small dose may be given to minimize side effects and then increased gradually (eg, 25% of the desired dose in week 1, 50% in week 2, and the full dose by week 3). Avoid if penicillin allergic. Monitor for proteinuria, hematuria, rash, leukopenia, thrombocytopenia.
3) BAL (Dimercaprol): Is indicated for patients with severe gastrointestinal symptoms or patients in renal failure. Administer 3 to 5 mg/kg/dose every 4 hours IM for the first 48 hours, then 2.5 to 3 mg/kg every 6 hours for the second 48 hours, then every 12 hours for 7 additional days.
4) DMPS: A chelating agent, available in Europe, for the treatment of arsenic, bismuth, lead, copper, and mercury toxicity. ADULT DOSE: IV: DAY 1: 250 mg every 3 to 4 hours (1500 to 2000 mg total); DAY 2: 250 mg every 4 to 6 hours (1000 to 1500 mg total); DAY 3: 250 mg every 6 to 8 hours (750 to 1000 mg total); DAY 4: 250 mg every 8 to 12 hours (500 to 750 mg total); SUBSEQUENT DAYS: 250 mg every 8 to 24 hours (250 to 750 mg total). ORAL: ACUTE TOXICITY: 1200 to 2400 mg/day in equally divided doses (100 to 200 mg 12 times daily); CHRONIC TOXICITY: 300 to 400 mg/day orally (in single doses of 100 to 200 mg). The dose may be increased in severe toxicity.

1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.

1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
2) Take precautions to avoid exposure of health care professionals and other individuals.
3) SYSTEMIC EFFECTS

1) Circulatory collapse can occur from mercury poisoning (Sittig, 1991) HSDB, 1999).

1) Severe and potentially fatal pulmonary edema can occur from inhalation of mercury (ILO, 1983). Because mercury is converted to mercuric ion in the body, mercuric salts could possibly cause similar effects.

1) Inhalation of high concentrations of mercury vapor can cause cough, dyspnea, chest pain, bronchitis, and pneumonitis (ACGIH, 1996).

1) Mercury crosses the blood-brain barrier (Blum & Manzo, 1985).

1) A neurological syndrome resembling amyotrophic lateral sclerosis (Lou Gehrig disease) can occur even from acute exposure to mercury and its salts (Adams et al, 1983). The peripheral effects involve a dying-back axonopathy, followed by demyelinization. General loss of brain function may also occur (Folkl & Konig, 1983).

1) Seizures may occur (Sittig, 1991).

1) Nausea, vomiting, and bloody diarrhea may occur from ingestion or inhalation of inorganic mercury salts (Clayton & Clayton, 1981).

1) Small bowel obstruction due to adhesions occurred in a case of ingestion of an alkaline disc battery containing mercuric oxide (Mant et al, 1987). In a study of 64 dogs, ingestion of disc batteries did not cause caustic injury to the GI tract because the battery casings remained intact (Litovitz et al, 1984).

1) Oliguria, anuria, and renal failure may occur (Sittig, 1991).

1) Contact with the skin may cause irritation and dermatitis (EPA, 1985; Sittig, 1991).

1) Fetotoxicity, post-implantation mortality and developmental abnormalities in the eye and ear have been observed in rat studies. In the mouse, fetal death and developmental abnormalities have been observed (RTECS, 1999).

1) HUMANS
2) ANIMALS

1) All forms of mercury move freely across the placenta, and fetal concentrations are at least as high as those in the mother (HSDB, 1999).

1) Increased spontaneous abortions, and menstrual dysfunction, have been reported in women exposed to mercury (Goncharuk, 1971; Panova & Ivanova, 1976; Goncharuk, 1977; Marinova, 1973).

1) INHALATION - Lien et al (1983) reported a case of acute mercury inhalation toxicity in a pregnant woman. Twenty-six days after the exposure the child was born without clinical abnormalities, but with serum blood levels comparable with the mother's.

1) Mercury is found in human breast milk (Mattison, 1983). Oral absorption of mercury is greater in infants than in adults (Barlow & Sullivan, 1982). A level of 4 mcg/L in breast milk is considered dangerous for infants (Mattison, 1983).
2) Gonzalez et al (1985) report a correlation between total mercury concentrations measured in the hair of nursing neonates and their mothers to be significant.

1) Not Listed

1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

1) LACK OF EFFECT

1) Normal whole blood mercury levels rarely exceed 1.5 mcg/dL in unexposed individuals. Normal levels are approximately 0.5 mcg/dL (Skerfving, 1972). Levels of 0.4 to 22 mcg/mL have been lethal (HSDB, 1999).
2) Most commonly used analytical methods do not distinguish between inorganic and organic mercury in the blood (Zenz, 1988). The use of blood mercury levels after acute exposure should be considered with the knowledge that a single seafood meal will elevate levels for 20 to 30 hours (Kershaw et al, 1980; Sherlock et al, 1984). Specific analysis of inorganic mercury in the blood did correlate with the level of exposure in workers exposed chronically (Yoshida, 1985).
3) In acute exposures, elevation of blood-mercury levels to ranges of 25 to 50 mcg/dL (1246.2 to 2492.5 nmol/L) precede elevations in urinary excretion because of the body's capacity to store mercury (Cherian et al, 1978).
4) Blood mercury levels did not correlate with indicators of toxicity in chronically exposed workers (Rosenman et al, 1986).

1) Normal urine excretion rarely exceeds 15 mcg/L (74.7 nmol/L) in unexposed individuals. Normal levels are approximately 0.5 mcg/L, with the upper limit of normality being 20 mcg/L (Clayton & Clayton, 1981). Levels of 0.1 to 0.5 mg Hg/L (100 to 500 mcg/L) are considered significantly elevated (Sittig, 1985).
2) Spot urine levels are inconsistent due to diurnal variation. The interpretation of these levels is most accurate when samples are taken at the same time of day and corrected for creatinine. Because proteinuria and glycosuria cause specific gravity changes, correction using this method is less accurate than the creatinine method. Patients with kidney damage should be excluded (Calder et al, 1984).
3) Monitoring of spot urine mercury levels did correlate with occurrence of neuropsychological toxicity and motor nerve conduction velocity in 42 chronically exposed workers (Rosenman et al, 1986).
4) Urine 24-hour delta ALA levels are invariably elevated to the ranges of 3 to 10 mg/liter in chronic poisoning cases. Although urinary levels as high as 2000 mcg/L have been seen without symptoms, levels greater than 100 mcg/L may need careful behavioral and neurological evaluation (Adams et al, 1983).
5) Workers chronically exposed to mercury vapor exhibited preclinical renal toxicity at spot urine mercury levels of greater than 50 mcg/g creatinine (Roels et al, 1985).
6) Collection of a 24-hour urine sample, followed by challenge with D-penicillamine for 4 days, has been used to document mercury body burden (Ishihara et al, 1974).

1) ELECTROPHYSIOLOGICAL TESTING
2) MONITORING
3) PULMONARY FUNCTION TESTS

1) Mercury salts may be corrosive but GI perforation is not common. The role of gastric decontamination is unclear.
2) Abdominal x-ray may be useful in evaluating the need for gastric lavage.

1) CHARCOAL ADMINISTRATION
2) CHARCOAL DOSE

1) CAUTION: Progressive pulmonary distress, leading to fatal cardiopulmonary arrest, was attributed to aspiration of mercury during unprotected gastric lavage following a large overdose of mercuric chloride. Elective tracheal intubation should be considered prior to performance of gastric lavage (McLauchlan, 1991).
2) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
3) PRECAUTIONS:
4) LAVAGE FLUID:
5) COMPLICATIONS:
6) CONTRAINDICATIONS:

1) Chelation should be performed with one of the following drugs in severe poisonings.
2) All of the effective complexing agents administered to facilitate removal of mercury from the body contain sulfhydryl groups (Clarkson, 1990).

1) INDICATION
2) DOSE
3) EFFICACY
4) LABORATORY
5) ADVERSE EFFECTS

1) USUAL ADULT DOSE
2) USUAL PEDIATRIC DOSE
3) ADVERSE REACTIONS
4) DURATION OF THERAPY
5) CAUTIONS
6) PREGNANCY
7) IMPAIRED RENAL FUNCTION
8) EFFICACY

1) SUCCIMER/DMSA/EFFICACY
2) SUCCIMER/DOSE/ADMINISTRATION
3) MONITORING PARAMETERS
4) SUCCIMER/ADVERSE EFFECTS: The following adverse events have occurred in children and adults during clinical trials: nausea, vomiting and diarrhea; transient liver enzyme elevations; rash, pruritus; drowsiness and paresthesia. Events reported infrequently include: sore throat, rhinorrhea, mucosal vesicular eruption, thrombocytosis, eosinophilia, and mild to moderate neutropenia (Prod Info CHEMET(R) oral capsules, 2011).
5) ODOR: Succimer has a sulfurous odor that may be evident in the patient's breath or urine (Prod Info CHEMET(R) oral capsules, 2005).
6) HYPERTHERMIA: One adult developed acute severe hyperthermia associated with hypotension; rechallenge resulted in hyperthermia with shaking chills and hypertension (Marcus et al, 1991).
7) AVAILABLE FORMS: Succimer (Chemet (R)), 100 mg capsules (Prod Info CHEMET(R) oral capsules, 2011).
8) Succimer has a sulfurous odor that may be evident in the patients' breath and urine (Prod Info, 1991a).

1) DOSE
2) EFFICACY
3) AVAILABILITY

1) DMPS/INDICATIONS: Chelating agent for heavy metal toxicities associated with arsenic, bismuth, copper, lead and mercury (Blanusa et al, 2005).
2) DMPS/DOSING
3) SOURCES
4) EFFICACY
5) ADVERSE REACTIONS

1) N-acetyl cysteine has been shown to protect against mercury-induced nephrotoxicity in animal models of inorganic mercury poisoning (Girardi & Elias, 1991).

1) There is little information regarding the use of endoscopy, corticosteroids or surgery in the setting of concentrated mercuric oxide ingestion. The following information is derived from experience with other corrosives.
2) SUMMARY: Obtain consultation concerning endoscopy as soon as possible, and perform endoscopy within the first 24 hours when indicated.
3) INDICATIONS: Endoscopy should be performed in adults with a history of deliberate ingestion, adults with any signs or symptoms attributable to inadvertent ingestion, and in children with stridor, vomiting, or drooling after unintentional ingestion (Crain et al, 1984). Endoscopy should also be performed in children with dysphagia or refusal to swallow, significant oral burns, or abdominal pain after unintentional ingestion (Gaudreault et al, 1983; Nuutinen et al, 1994). Children and adults who are asymptomatic after accidental ingestion do not require endoscopy (Gupta et al, 2001; Lamireau et al, 2001; Gorman et al, 1992).
4) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
5) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):
6) GRADING
7) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.
8) SCINTIGRAPHY - Scans utilizing radioisotope labelled sucralfate (technetium 99m) were performed in 22 patients with caustic ingestion and compared with endoscopy for the detection of esophageal burns. Two patients had minimal residual isotope activity on scanning but normal endoscopy and two patients had normal activity on scan but very mild erythema on endoscopy. Overall the radiolabeled sucralfate scan had a sensitivity of 100%, specificity of 81%, positive predictive value of 84% and negative predictive value of 100% for detecting clinically significant burns in this population (Millar et al, 2001). This may represent an alternative to endoscopy, particularly in young children, as no sedation is required for this procedure. Further study is required.
9) MINIPROBE ULTRASONOGRAPHY - was performed in 11 patients with corrosive ingestion . Findings were categorized as grade 0 (distinct muscular layers without thickening, grade I (distinct muscular layers with thickening), grade II (obscured muscular layers with indistinct margins) and grade III (muscular layers that could not be differentiated). Findings were further categorized as to whether the worst appearing image involved part of the circumference (type a) or the whole circumference (type b). Strictures did not develop in patients with grade 0 (5 patients) or grade I (4 patients) lesions. Transient stricture formation developed in the only patient with grade IIa lesions, and stricture requiring repeated dilatation developed in the only patient with grade IIIb lesions (Kamijo et al, 2004).

1) CORROSIVE INGESTION/SUMMARY: The use of corticosteroids for the treatment of caustic ingestion is controversial. Most animal studies have involved alkali-induced injury (Haller & Bachman, 1964; Saedi et al, 1973). Most human studies have been retrospective and generally involve more alkali than acid-induced injury and small numbers of patients with documented second or third degree mucosal injury.
2) FIRST DEGREE BURNS: These burns generally heal well and rarely result in stricture formation (Zargar et al, 1989; Howell et al, 1992). Corticosteroids are generally not beneficial in these patients (Howell et al, 1992).
3) SECOND DEGREE BURNS: Some authors recommend corticosteroid treatment to prevent stricture formation in patients with a second degree, deep-partial thickness burn (Howell et al, 1992). However, no well controlled human study has documented efficacy. Corticosteroids are generally not beneficial in patients with a second degree, superficial-partial thickness burn (Caravati, 2004; Howell et al, 1992).
4) THIRD DEGREE BURNS: Some authors have recommended steroids in this group as well (Howell et al, 1992). A high percentage of patients with third degree burns go on to develop strictures with or without corticosteroid therapy and the risk of infection and perforation may be increased by corticosteroid use. Most authors feel that the risk outweighs any potential benefit and routine use is not recommended (Boukthir et al, 2004; Oakes et al, 1982; Pelclova & Navratil, 2005).
5) CONTRAINDICATIONS: Include active gastrointestinal bleeding and evidence of gastric or esophageal perforation. Corticosteroids are thought to be ineffective if initiated more than 48 hours after a burn (Howell, 1987).
6) DOSE: Administer daily oral doses of 0.1 milligram/kilogram of dexamethasone or 1 to 2 milligrams/kilogram of prednisone. Continue therapy for a total of 3 weeks and then taper (Haller et al, 1971; Marshall, 1979). An alternative regimen in children is intravenous prednisolone 2 milligrams/kilogram/day followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks then tapered (Anderson et al, 1990).
7) ANTIBIOTICS: Animal studies suggest that the addition of antibiotics can prevent the infectious complications associated with corticosteroid use in the setting of caustic burns. Antibiotics are recommended if corticosteroids are used or if perforation or infection is suspected. Agents that cover anaerobes and oral flora such as penicillin, ampicillin, or clindamycin are appropriate (Rosenberg et al, 1953).
8) STUDIES

1) SUMMARY: Initially if severe esophageal burns are found a string may be placed in the stomach to facilitate later dilation. Insertion of a specialized nasogastric tube after confirmation of a circumferential burn may prevent strictures. Dilation is indicated after 2 to 4 weeks if strictures are confirmed. If dilation is unsuccessful colonic intraposition or gastric tube placement may be needed. Early laparotomy should be considered in patients with evidence of severe esophageal or gastric burns on endoscopy.
2) STRING - If a second degree or circumferential burn of the esophagus is found a string may be placed in the stomach to avoid false channel and to provide a guide for later dilation procedures (Gandhi et al, 1989).
3) STENT - The insertion of a specialized nasogastric tube or stent immediately after endoscopically proven deep circumferential burns is preferred by some surgeons to prevent stricture formation (Mills et al, 1978; (Wijburg et al, 1985; Coln & Chang, 1986).
4) DILATION - Dilation should be performed at 1 to 4 week intervals when stricture is present(Gundogdu et al, 1992). Repeated dilation may be required over many months to years in some patients. Successful dilation of gastric antral strictures has also been reported (Hogan & Polter, 1986; Treem et al, 1987).
5) COLONIC REPLACEMENT - Intraposition of colon may be necessary if dilation fails to provide an adequate sized esophagus (Chiene et al, 1974; Little et al, 1988; Huy & Celerier, 1988).
6) LAPAROTOMY/LAPAROSCOPY - Several authors advocate laparotomy or laparoscopy in patients with endoscopic evidence of severe esophageal or gastric burns to evaluate for the presence of transmural gastric or esophageal necrosis (Cattan et al, 2000; Estrera et al, 1986; Meredith et al, 1988; Wu & Lai, 1993).

1) SUMMARY
2) DIAZEPAM
3) NO INTRAVENOUS ACCESS
4) LORAZEPAM
5) PHENOBARBITAL
6) OTHER AGENTS

1) Acute inhalation exposure to mercury compounds can produce local effects on the pulmonary system and can produce elevated urine mercury concentrations (Levin et al, 1988). Chelation may be required.
2) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
3) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
4) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
5) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
6) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
7) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
8) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).

1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

1) In cases of significant exposure prehospital decontamination should occur outside the medical facility if possible since the wash may contaminate medical personnel and cause them to become poisoned.
2) Remove all contaminated clothing, seal into bags, and treat as hazardous waste. The person performing decontamination may be protected by wearing rubber gloves, disposable shoe covers, and a rubber apron.
3) All medical personnel should wear protective clothing, including respirators if significant amounts of dust are present, to prevent secondary contamination.

1) APPLICATION
2) DEBRIDEMENT
3) TREATMENT
4) TETANUS PROPHYLAXIS

1) Carefully observe patients with DERMAL exposure for the development of any systemic signs or symptoms.

a) The total amount of mercury removed (1189 mg) was less than 0.1 percent of the estimated ingested dose (1425 mg) of mercuric chloride, and the patient died 28 days postingestion.

a) Children are more susceptible than adults to mercury poisoning (HSDB, 1999).

a) Threshold concentration for fresh and saltwater fish, 0.01 ppm (OHM/TADS, 1999).
b) 3 grams of mercury may be fatal to humans.
c) 75 milligrams per day in drinking water would be lethal; 50 parts per million in water can be toxic (OHM/TADS, 1999)

1) LD50- (INTRAPERITONEAL)MOUSE:
2) LD50- (ORAL)MOUSE:
3) LD50- (ORAL)RAT:
4) LD50- (SKIN)RAT: