Mercuric Nitrate

CAS RN: 10045-94-0

Treatment Overview

0.4.2 ORAL/PARENTERAL EXPOSURE
  • A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    • 1) Supportive care with intravenous fluid resuscitation for gastrointestinal losses and antiemetics for nausea and vomiting should be initiated following clinically significant acute ingestions. Chelation therapy should be given to patients with significant exposures.
  • B) MANAGEMENT OF SEVERE TOXICITY
    • 1) Fluid resuscitation with isotonic fluids to replace gastrointestinal fluid losses and treat hypotension should be initiated immediately. When the patient is felt to be euvolemic, vasopressors can be added for persistent hypotension. Chelation therapy should be started as soon as possible.
  • C) DECONTAMINATION
    • 1) PREHOSPITAL: Dermal exposures should be washed off with soap and water. Prehospital gastrointestinal decontamination is not indicated.
    • 2) HOSPITAL: Inorganic mercury is poorly absorbed through the gastrointestinal tract thus small ingestions do not warrant gastrointestinal decontamination. Large ingestions accompanied by poor gut motility that present early may benefit from activated charcoal and gastric lavage. Whole bowel irrigation may be necessary in patients with persistent radiographic evidence of mercury in the gastrointestinal tract.
  • D) AIRWAY MANAGEMENT
    • 1) Airway management may be necessary if a patient develops significant hypoxia due to pneumonitis or if the patient requires airway protection to facilitate endoscopic evaluation or gastrointestinal decontamination.
  • E) ANTIDOTE
    • 1) None.
  • F) CHELATION
    • 1) Parenteral chelation (intramuscular Dimercaprol (BAL) or intravenous unithiol) therapy should be initiated in patients with significant acute exposures (any patient with gastrointestinal symptoms after acute exposure or history of a deliberate or significant ingestion). BAL is given in decreasing doses over 10 days if the patient is unable to take oral medications. The dosing schedule is as follows: 5 mg/kg initially, followed by 2.5 mg/kg 1 or 2 times daily for 10 days. When the patient is able to tolerate oral medications, BAL can be replaced with succimer with no waiting period between treatments. Succimer may given based on the following dosing schedule:
    • 1) 10 mg/kg orally 3 times daily for 5 days then
    • 2) 10 mg/kg 2 times daily for 14 days. Succimer may be used alone in chronically exposed patients without gastrointestinal toxicity. Unithiol (2,3-dimercaptopropanol-sulfonic acid, DMPS) is available through compounding pharmacies in the United States. It is a water-soluble analog of BAL, and can be given orally or parenterally. It is considered a better mercury chelator than succimer. Unithiol is dosed as follows: IV: Day one 250 mg/kg every 3 to 4 hours, day two 250 mg every 4 to 6 hours, day three 250 mg every 6 to 8 hours, day four 250 mg every 8 to 12 hours, days five and six: 250 mg every 8 to 24 hours. ORAL: Initially 1200 mg to 2400 mg every 24 hours divided (100 mg or 200 mg every 2 hours), reduce to 100 mg to 300 mg every 8 hours as tolerated. Depending on the patient's clinical status, therapy may be changed to the oral route after the fifth day: 100 to 300 mg 3 times daily. Patients should be treated for 14 days or until there is no mercury detected in the urine.
  • G) ENHANCED ELIMINATION
    • 1) There is no role for hemodialysis or hemoperfusion in the elimination of inorganic mercury from the body. However, hemodialysis may be necessary due to renal failure.
  • H) PATIENT DISPOSITION
    • 1) HOME CRITERIA: Asymptomatic patients with small inadvertent exposures and without vomiting may be managed at home.
    • 2) OBSERVATION CRITERIA: Patients with small exposures without significant caustic effects or gastrointestinal toxicity may be observed for 8 hours. If the patient can take oral food and fluids without discomfort, they have normal renal function and urinalysis at the end of observation, then they may be discharged.
    • 3) ADMISSION CRITERIA: Any patients with vomiting or diarrhea, caustic effects from ingestion, renal insufficiency, or other systemic toxicity should be admitted to the hospital for toxicology consultation and evaluation for chelation.
    • 4) CONSULT CRITERIA: Patients with presumed gastrointestinal caustic injury should be evaluated by a gastroenterologist for endoscopic evaluation of the injuries. A toxicologist should be consulted in cases of acute ingestion, or cases in which the patient has developed renal insufficiency, caustic injury, or other systemic manifestation felt to be secondary to inorganic mercury.
  • I) PITFALLS
    • 1) Insufficient fluid resuscitation can result in progression to multi-organ dysfunction. Failure to identify the source of mercury exposure may lead to on-going exposure. If patients are not chelated expeditiously when significant exposure has occurred, renal failure will ensue. Early chelation may prevent or minimize renal injury.
  • J) TOXICOKINETICS
    • 1) Inorganic mercury is primarily absorbed through the gastrointestinal tract; expected absorption is only 10% of the ingested dose. Dermal absorption is possible. It is usually due to chronic exposure and is facilitated by high mercury concentration, exposure to excoriated or damaged dermis, and high lipid solubility of the carrier. Significant inhalational exposure is rare but possible. Inorganic mercury is primarily excreted through the kidneys though diffusion into the gastrointestinal tract does contribute to body elimination. The half-life of inorganic mercury is estimated to be 30 to 60 days.
  • K) DIFFERENTIAL DIAGNOSIS
    • 1) Arsenic may cause a similar caustic gastroenteritis accompanied by renal injury. Other caustic ingestions should be considered. Methylxanthines (caffeine or theophylline) cause a presentation with profound gastroenteritis though these patients will often have seizures and hypokalemia. Renal insufficiency is not expected in methylxanthine toxicity unless large fluid losses lead to a pre-renal acute tubular necrosis. Very large non-steroidal anti-inflammatory overdoses may lead to significant gastrointestinal toxicity, renal insufficiency, and acidosis. Infectious gastroenteritis may cause enough fluid loss to cause an acute tubular necrosis due to hypovolemia.
0.4.3 INHALATION EXPOSURE
  • A) Bronchodilators and oxygen therapy should be provided to patients with bronchospasm or pneumonitis.
0.4.4 EYE EXPOSURE
  • A) Gross removal of salts and foreign bodies from conjunctiva should be attempted with a moistened Q-tip. Do no wipe cornea directly with Q-tip due to the risk of corneal abrasion. Irrigation with isotonic fluid 1 to 2 Liters should be performed to remove smaller debris and normalize pH.
0.4.5 DERMAL EXPOSURE
  • A) OVERVIEW
    • 1) Decontaminate with soap and water. Treat caustic injuries with topical wound care ointments, such as 1% silver sulfadiazine cream (silvadene).
    • 2) Take precautions to avoid exposure of health care professionals and other individuals.
    • 3) Initiate chelation therapy in patients with systemic effects
0.4.2 ORAL EXPOSURE
  • A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    • 1) Treatment of mild to moderate toxicity consists of predominantly symptomatic and supportive care. Patients with mild hypotension should be treated with IV fluid hydration.
  • B) MANAGEMENT OF SEVERE TOXICITY
    • 1) Patients who develop severe hypotension should be treated first with aggressive IV fluid hydration. Vasopressors should be used with caution as they intensify the arteriolar constriction that is generated by spontaneous reflexes in the nitrite-poisoned patient, thereby further compromising tissue blood flow. METHEMOGLOBINEMIA: Symptomatic patients should be treated with methylene blue. Rarely, pediatric patients with severe methemoglobinemia not responsive to methylene blue therapy may require exchange transfusion; patients may be temporized while awaiting transfusion with hyperbaric oxygen therapy. SEIZURES: Treat seizures with benzodiazepines; add barbiturates if seizures persist.
  • C) DECONTAMINATION
    • 1) PREHOSPITAL: Prehospital gastrointestinal decontamination is generally not recommended because of the potential for CNS depression or persistent seizures and subsequent aspiration.
    • 2) HOSPITAL: Gastrointestinal decontamination with single-dose activated charcoal may be considered in patients with a recent (within 1 hour) potentially life-threatening ingestion of sodium nitrite who are awake and able to protect their airway.
  • D) AIRWAY MANAGEMENTS
    • 1) Patients with nitrite toxicity may require intubation for respiratory failure associated with altered mental status due to hypotension or functional hypoxia due to methemoglobinemia.
  • E) ANTIDOTE
    • 1) There is no specific antidote for treatment of nitrite toxicity. However, patients who develop significant methemoglobinemia (symptomatic patients or patients with a methemoglobin level of greater than 30%) should be treated with methylene blue. Contraindications to treatment with methylene blue include known G-6-PD deficiency (may cause hemolysis), known hypersensitivity to methylene blue, and methemoglobin reductase deficiency.
  • F) METHEMOGLOBINEMIA
    • 1) Initiate oxygen therapy. Treat with methylene blue if patient is symptomatic (usually at methemoglobin concentrations greater than 20% to 30% or at lower concentrations in patients with anemia, underlying pulmonary or cardiovascular disease). METHYLENE BLUE: INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules and 10 mg/1 mL (1% solution) vials. Additional doses may sometimes be required. Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection. NEONATES: DOSE: 0.3 to 1 mg/kg.
  • G) ENHANCED ELIMINATION
    • 1) Hemodialysis is typically not useful for treatment of nitrite toxicity. Exchange transfusion may be considered in severely symptomatic patients, especially neonatal and pediatric patients, if the methemoglobinemia is not responsive to methylene blue therapy. It may also be useful in patients with known G-6-PD deficiency or NADPH-dependent methemoglobin reductase deficiencies. Exchange transfusions are of limited applicability in adults due to the inherent risks of large blood volumes required in adults. Although there is limited data in humans, hyperbaric oxygen (HBO) may be considered as a supportive measure while preparations for exchange transfusion are being made. HBO may provide sufficient oxygen to maintain life with dissolved oxygen in blood, and temporarily obviates the need for functional hemoglobin.
  • H) PATIENT DISPOSITION
    • 1) OBSERVATION CRITERIA: Patients with deliberate or significant exposure should be sent to a healthcare facility for evaluation, treatment, and observation. Patients who are asymptomatic with normal methemoglobin concentrations can be discharged after 6 hours of observation.
    • 2) ADMISSION CRITERIA: Patients who develop significant hypotension, or signs and symptoms of methemoglobinemia should be admitted to an intensive care unit.
    • 3) CONSULT CRITERIA: Contact a local poison center for a toxicology consult for any patient with suspected symptomatic nitrite toxicity.
  • I) PITFALLS
    • 1) The arterial pO2 is usually normal despite significant methemoglobinemia. Pulse oximetry may overestimate oxygen saturation in patients with significant methemoglobinemia and should not be used to reflect arterial oxygen content or tissue oxygen delivery. Ongoing absorption can lead to recurrent methemoglobinemia.
  • J) PHARMACOKINETICS
    • 1) Simple aliphatic nitrites such as ethyl nitrite, isobutyl nitrite, and amyl nitrite are volatile liquids readily absorbed through the lungs. Sodium nitrite is readily absorbed through the GI tract after ingestion, and is commonly given medically intravenously. Approximately 60% of nitrite ions are metabolized, with ammonia as one of the end products; 40% of nitrite is excreted unchanged in the urine.
  • K) DIFFERENTIAL DIAGNOSIS
    • 1) The differential for nitrite toxicity includes other causes of vasodilatory hypotension, other causes of methemoglobinemia, and in the setting of sodium nitrite treatment for cyanide poisoning, includes the underlying cyanide toxicity.
0.4.3 INHALATION EXPOSURE
  • A) Move patient to fresh air. Monitor for respiratory distress. Administer oxygen and assist ventilation as required.
0.4.4 EYE EXPOSURE
  • A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
0.4.5 DERMAL EXPOSURE
  • A) OVERVIEW
    • 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).
    • 2) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
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