Calcium Nitrate

CAS RN:10124-37-5

Treatment Overview

0.4.2 ORAL EXPOSURE
  • A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    • 1) There is no specific antidote for calcium salts poisoning. Most cases of hypercalcemia can be treated with saline hydration. Gastrointestinal or skin irritation is usually self-limited and does not require specific treatment beyond decontamination. There is no role for bisphosphonates or calcitonin in the treatment of hypercalcemia due to calcium salt exposure.
  • B) MANAGEMENT OF SEVERE TOXICITY
    • 1) Most cases of hypercalcemia will resolve with hydration in patients with normal renal function. Hemodialysis can be used if emergent clearance is required of if the patient's renal function is impaired. There is no role for bisphosphonates or calcitonin in the treatment of hypercalcemia due to calcium salt exposure.
  • C) DECONTAMINATION
    • 1) PREHOSPITAL: DERMAL EXPOSURE: Remove clothes and wash the body with copious amounts of water following dermal exposure to caustic salts.
    • 2) HOSPITAL: Gastric decontamination is not indicated for ingestion of salts. Patients who ingest caustic salts should rinse their mouth and may ingest a small amount (30 to 60 mL) of water.
  • D) ANTIDOTE
    • 1) There is no antidote for calcium salts.
  • E) EXTRAVASATION INJURY
    • 1) If extravasation occurs, stop the infusion. Disconnect the IV tubing, but leave the cannula or needle in place. Attempt to aspirate the extravasated drug from the needle or cannula. If possible, withdraw 3 to 5 mL of blood and/or fluids through the needle/cannula. Administer hyaluronidase (see below). Elevate the affected area. Apply warm packs for 15 to 20 minutes at least 4 times daily. Administer analgesia for severe pain. If pain persists, there is concern for compartment syndrome, or injury is apparent, an early surgical consult should be considered. Close observation of the extravasated area is suggested. If tissue sloughing, necrosis or blistering occurs, treat as a chemical burn (ie, antiseptic dressings, silver sulfadiazine, antibiotics when applicable). Surgical or enzymatic debridement may be required. Risk of infection is increased in chemotherapy patients with reduced neutrophil count following extravasation. Consider culturing any open wounds. Monitor the site for the development of cellulitis, which may require antibiotic therapy.
  • F) ENHANCED ELIMINATION PROCEDURE
    • 1) Calcium is rapidly cleared by hemodialysis. However, dialysis is rarely indicated unless the patient has renal failure.
  • G) PATIENT DISPOSITION
    • 1) HOME CRITERIA: A patient who is asymptomatic or has mild GI irritation after an inadvertent exposure can be observed at home.
    • 2) OBSERVATION CRITERIA: A symptomatic patient and/or those with a deliberate overdose should be evaluated in a healthcare facility.
    • 3) ADMISSION CRITERIA: Patients who have high serum calcium concentrations that do not improve with hydration, or have concomitant renal insufficiency, should be admitted for hydration and monitoring.
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.
Find more information on this substance at: Hazardous Substances Data Bank , TOXNET , PubMed