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SILVER NITRATE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Sodium nitrate is a colorless, odorless, crystalline (sugar-like) solid, produced synthetically by reacting nitric acid with sodium carbonate.

Specific Substances

    1) Argenti Nitras
    2) Argent Nit
    3) Argentum Nitricum
    4) Nitrato de Plata
    5) CAS 7761-88-8
    6) LUNAR CAUSTIC
    7) NITRATE D'ARGENT (FRENCH)
    8) NITRIC ACID, SILVER(H) SALT
    9) SILBERNITRAT
    10) SILVER(H) NITRATE

Available Forms Sources

    A) FORMS
    1) Ophthalmic Solution: Silver nitrate 1% (Kastrup, 1988)
    2) Topical Preparations (Kastrup, 1988)
    a) Solutions
    1) Silver nitrate 10%, 30 mL
    2) Silver nitrate 25%, 30 mL
    3) Silver nitrate 50%, 30 mL
    b) Ointment: Silver nitrate 10%, 30 g
    3) Mild Silver Protein (Kastrup, 1988)
    a) 10% solution (20 mg/mL silver)
    b) 20% ophthalmic solution
    4) Silver nitrate sticks contain 75% silver nitrate and 25% potassium permanganate (Stokinger, 1981).
    B) USES
    1) Silver nitrate is used in the manufacture of silver chloride, photographic sensitive materials, photographic plating, mirrors, catalysts, and pharmaceuticals. It may also be used in photographic dark rooms.
    2) A 1% silver nitrate solution has been instilled into the eyes of newborns immediately after birth to prevent gonorrheal ophthalmia neonatorum (Kastrup, 1988).
    3) Silver nitrate 10% is used in podiatry to treat helomas and in dermatology to treat pruritus and impetigo vulgaris (Kastrup, 1988).
    4) Silver nitrate 25% solution is used to treat pruritus and plantar warts (Kastrup, 1988).
    5) Silver nitrate 50% solution is used in the treatment of granuloma pyogenicum, papillomatous growths, granulation tissue, and plantar warts (Kastrup, 1988).
    6) Silver nitrate 0.1% to 0.5% has an unlabeled use as wet dressings in burns or lesions (Kastrup, 1988).
    7) Mild silver protein 10% solution is used in mild inflammatory conditions of the eye, ear, nose, throat, rectum, urethra, and vagina (Kastrup, 1988).
    8) Mild silver protein 20% ophthalmic solution is used in eye infections and postoperatively in eye surgery (Kastrup, 1988).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) BACKGROUND: Sodium nitrate is a colorless, odorless, crystalline (sugar-like) solid, produced synthetically by reacting nitric acid with sodium carbonate.
    B) USES: MEDICINAL: Silver nitrate has been used for various conditions including burns, plantar warts, and mild inflammatory conditions of the eye, ear, nose, throat, rectum, urethra, and vagina. In low concentrations it is used as an antibacterial agent. It has been combined with sodium sulfadiazine to create silver sulfadiazine (SSD) cream used topically to treat burns. Concentrations of silver nitrate greater than 1% have astringent, irritant, or caustic properties. Solutions of 10% up to 25% have been used to treat pruritus, impetigo vulgaris and plantar warts and solutions of 50% have been used in the treatment of granuloma pyogenicum, papillomatous growths, granulation tissue, and plantar warts. INDUSTRY: Silver nitrate is used in the manufacture of silver chloride, photographic sensitive materials, photographic plating, mirrors, catalysts, and pharmaceuticals. It may also be used in photographic dark rooms.
    C) PHARMACOLOGY: Silver has bactericidal activity. Silver nitrate in concentrations between 0.5% and 1% are used as antibacterial agents. Concentrations of silver nitrate greater than 1% have astringent, irritant, or caustic properties.
    D) EPIDEMIOLOGY: Exposure has occurred. Overdose is uncommon.
    E) WITH THERAPEUTIC USE
    1) ADVERSE EVENTS: Silver nitrate is a skin irritant that may cause dermatitis, rashes, burns, or argyria (if exposures are chronic). Hypochloremia and associated hyponatremia may be seen due to reaction with chloride. Corneal opacification and bleeding conjunctiva have developed in newborns following the instillation of silver nitrate drops. Methemoglobinemia was noted in several burn patients who were treated with silver nitrate.
    F) WITH POISONING/EXPOSURE
    1) OVERDOSE: Silver nitrate is a skin irritant that may cause dermatitis, rashes, burns, or argyria (if exposures are chronic). It is a strong mucous membrane irritant-corrosive. Toxicity may be due to its silver component (argyria), its nitrate component (methemoglobinemia), and its corrosive nature. Silver nitrate is also a strong caustic and can cause tissue damage and necrosis. Silver can be absorbed predominantly through mucous membranes and burn wound surfaces. The irritant, astringent, or corrosive properties of silver nitrate are dependent on the concentration and duration of exposure.
    2) INGESTION: Nausea, vomiting, and abdominal pain, as well as diarrhea may occur after ingestion. Dizziness and seizures have been observed after oral ingestions.
    3) INHALATION: The dust is a pulmonary irritant.
    0.2.4) HEENT
    A) WITH POISONING/EXPOSURE
    1) Silver nitrate is irritating to all mucous membranes including those of the gingiva, throat, mouth, and eyes. Dust is an eye irritant. Blindness may result if this chemical (high concentrations) is placed directly in the eye.

Laboratory Monitoring

    A) Monitor urea and electrolytes in symptomatic patients.
    B) Monitor methemoglobin levels in patients with symptoms of systemic absorption of silver nitrate or the presence of cyanosis.
    C) Following ingestion or suspected oral exposure to silver nitrate, endoscopy may be considered to rule out caustic injury.
    D) Obtain a baseline chest x-ray in a patient experiencing respiratory difficulties following an inhalation exposure.
    E) Obtain an ophthalmologic examination in patients with ocular symptoms after exposure to silver nitrate. It can also be used to detect exposure to silver nitrate as seen by deposits of silver in the eye by slit-lamp examination.
    F) Background serum levels of silver vary considerably but range from 0.04 mcg/g of blood to 0.3 mcg/g.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. Monitor vital signs. INGESTION: Perform oral exam to assess for mucous membrane injury. A minor "taste" ingestions of silver nitrate may only require dilution. If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting. Nausea and vomiting may develop following ingestion; monitor fluid status. Consider an endoscopy for a significant or suspected ingestion to assess for caustic injury. DERMAL: Remove contaminated clothing and copiously wash area with soap and water. Monitor electrolytes and/or methemoglobin level in patients with evidence of systemic injury. OCULAR: Copious irrigation; perform slit lamp exam. Consider Ophthalmology consult for persistent symptoms. ARGYRIA: If argyria develops, there is no effective treatment. Chelation therapy has not been found to be effective.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. INGESTION: Endoscopy should be performed as needed in any patient with a silver nitrate ingestion and evidence of caustic injury. Early airway management in patients with upper airway edema or respiratory distress. SEIZURES: Treat seizures with IV benzodiazepines, barbiturates. METHEMOGLOBINEMIA: Determine the methemoglobin concentration. Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations). Administer oxygen while preparing for methylene blue therapy.
    C) DECONTAMINATION
    1) PREHOSPITAL: Esophagoscopy may be indicated due to the caustic nature of silver nitrate. In this setting, activated charcoal may obscure endoscopy findings. Activated charcoal is NOT recommended in patients in whom significant gastrointestinal burns are likely (eg, presence of oral burns, persistent vomiting, drooling or stridor after ingestion).
    2) HOSPITAL: Dilution may be indicated in patients that can tolerate fluids. Activated charcoal is NOT recommended in patients in whom significant gastrointestinal burns are likely (eg, presence of oral burns, persistent vomiting, drooling or stridor after ingestion).
    D) AIRWAY MANAGEMENT
    1) Airway support is unlikely to be necessary following a mild topical exposure with no signs of systemic toxicity. Aggressive airway management may be necessary in patients with a deliberate ingestion or any indication of upper airway injury. The presence of edema may make intubation difficult. An inhalation injury may produce respiratory difficulties resulting in pneumonitis or pulmonary edema; monitor respiratory function. Oxygen therapy as needed. Ensure adequate ventilation and perform mechanical intubation as needed.
    E) ANTIDOTE
    1) Chelators are ineffective in treating argyria or the other effects of silver toxicity.
    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) ARGYRIA
    1) There has been some success with hydroquinone (5%) to treat argyria. SELENIUM and SULFUR: These agents have been considered for the treatment of argyria. Selenium may act to precipitate or chelate silver; it is theorized that an increase in selenium intake can bind with silver for excretion rather than being deposited in the skin
    H) ENHANCED ELIMINATION
    1) Enhanced elimination is unlikely to be necessary.
    I) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with an ingestion or a suspected ingestion of silver nitrate should be sent to a health care facility for evaluation. Patients with an endoscopic evaluation that demonstrates no burns or only a minor grade I burn(s), and who can tolerate oral intake can be discharged home.
    2) OBSERVATION CRITERIA: Patients with a deliberate acute ingestion should be monitored for signs and symptoms of caustic injury. Endoscopy should be performed as necessary.
    3) ADMISSION CRITERIA: Symptomatic patients, and those with endoscopically demonstrated grade II or higher burns should be admitted. Patients with evidence of respiratory distress, seizures, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting.
    4) CONSULT CRITERIA: Consult a hospital intensivist in patients requiring intensive care admission. Consult an ophthalmologist for patients with persistent ocular symptoms following irrigation.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    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) There have been a few cases of methemoglobinemia which have resulted from treatment of burn patients with silver nitrate, and if silver nitrate is to be used for burns, patients should be monitored for methemoglobinemia.
    2) 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).

Range Of Toxicity

    A) TOXICITY: ACUTE TOXICITY: The estimated acute oral fatal dose is approximately 10 g (form not specified) but 30 g has been survived. Silver nitrate is a strong irritant and would be expected to cause strong irritation or burns on skin and mucous membranes. ARGYRIA: On the average, argyria occurs after administration of 1 g of elemental silver by injection or 3.8 g of orally administered silver. METHEMOGLOBINEMIA: The most likely mechanism is conversion of nitrate to nitrite by organisms at the burn site resulting in methemoglobinemia in some patients. In severe cases, it may lead also lead to cyanosis and death.

Clinical Effects

Summary Of Exposure

    A) BACKGROUND: Sodium nitrate is a colorless, odorless, crystalline (sugar-like) solid, produced synthetically by reacting nitric acid with sodium carbonate.
    B) USES: MEDICINAL: Silver nitrate has been used for various conditions including burns, plantar warts, and mild inflammatory conditions of the eye, ear, nose, throat, rectum, urethra, and vagina. In low concentrations it is used as an antibacterial agent. It has been combined with sodium sulfadiazine to create silver sulfadiazine (SSD) cream used topically to treat burns. Concentrations of silver nitrate greater than 1% have astringent, irritant, or caustic properties. Solutions of 10% up to 25% have been used to treat pruritus, impetigo vulgaris and plantar warts and solutions of 50% have been used in the treatment of granuloma pyogenicum, papillomatous growths, granulation tissue, and plantar warts. INDUSTRY: Silver nitrate is used in the manufacture of silver chloride, photographic sensitive materials, photographic plating, mirrors, catalysts, and pharmaceuticals. It may also be used in photographic dark rooms.
    C) PHARMACOLOGY: Silver has bactericidal activity. Silver nitrate in concentrations between 0.5% and 1% are used as antibacterial agents. Concentrations of silver nitrate greater than 1% have astringent, irritant, or caustic properties.
    D) EPIDEMIOLOGY: Exposure has occurred. Overdose is uncommon.
    E) WITH THERAPEUTIC USE
    1) ADVERSE EVENTS: Silver nitrate is a skin irritant that may cause dermatitis, rashes, burns, or argyria (if exposures are chronic). Hypochloremia and associated hyponatremia may be seen due to reaction with chloride. Corneal opacification and bleeding conjunctiva have developed in newborns following the instillation of silver nitrate drops. Methemoglobinemia was noted in several burn patients who were treated with silver nitrate.
    F) WITH POISONING/EXPOSURE
    1) OVERDOSE: Silver nitrate is a skin irritant that may cause dermatitis, rashes, burns, or argyria (if exposures are chronic). It is a strong mucous membrane irritant-corrosive. Toxicity may be due to its silver component (argyria), its nitrate component (methemoglobinemia), and its corrosive nature. Silver nitrate is also a strong caustic and can cause tissue damage and necrosis. Silver can be absorbed predominantly through mucous membranes and burn wound surfaces. The irritant, astringent, or corrosive properties of silver nitrate are dependent on the concentration and duration of exposure.
    2) INGESTION: Nausea, vomiting, and abdominal pain, as well as diarrhea may occur after ingestion. Dizziness and seizures have been observed after oral ingestions.
    3) INHALATION: The dust is a pulmonary irritant.

Heent

    3.4.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Silver nitrate is irritating to all mucous membranes including those of the gingiva, throat, mouth, and eyes. Dust is an eye irritant. Blindness may result if this chemical (high concentrations) is placed directly in the eye.
    3.4.2) HEAD
    A) WITH THERAPEUTIC USE
    1) Necrotizing, ulcerative GINGIVITIS has been reported to occur after treating the gingiva with silver nitrate (Fletcher, 1976).
    3.4.3) EYES
    A) WITH THERAPEUTIC USE
    1) Corneal opacification and bleeding conjunctiva have been seen within one hour after application of 2 drops from a silver nitrate stick into the eyes of a newborn (Hornblass, 1975).
    2) CASE REPORT: CORNEAL INJURY was reported in a 42-year-old following application of a silver nitrate stick to her eyelid for hemostasis after a chalazion had been incised and drained (Stein et al, 1987).
    3) CASE REPORT: CORNEAL INJURY was reported in a newborn who received silver nitrate prophylaxis for ophthalmia neonatorum. On the 18th postnatal day a lamellar keratectomy removed stromal opacifications caused by the silver nitrate burn. There was no information available for follow-up on the status of the child's vision after this incident (Schirner et al, 1990).
    B) WITH POISONING/EXPOSURE
    1) The dust is an eye irritant (ITI, 1985; Grant, 1986).
    2) Blindness may result (Stokinger, 1981).
    3) Application of solutions greater than 2 percent have been associated with ocular damage (Stokinger, 1981).
    4) A blue-gray discoloration of the eyes may occur with chronic exposure to silver nitrate (ACGIH, 1980).
    3.4.5) NOSE
    A) WITH THERAPEUTIC USE
    1) Sneezing and rhinorrhea have been reported in patients treated with silver nitrate-tipped sticks for epistaxis.
    2) CASE REPORT: A 67-year-old immunocompromised patient developed a severe mucocutaneous reaction to silver nitrate cautery for recurrent minor epistaxis from both nostrils (Murthy & Laing, 1996).
    3) CASE REPORT: A 72-year-old developed a silver tattoo of the nasal mucosa after silver nitrate cautery. Silver tattoos can mimic melanomas in appearance (Mayall & Wild, 1996).
    3.4.6) THROAT
    A) WITH THERAPEUTIC USE
    1) Ulcerative GINGIVITIS occurred from application of silver nitrate to the gingiva (Fletcher, 1976).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) BRONCHITIS
    1) WITH POISONING/EXPOSURE
    a) The dust is a pulmonary irritant (ITI, 1985). Mild bronchitis was reported in 2 workers involved in the manufacture of silver nitrate (Rosenman et al, 1979).
    b) Mild chronic bronchitis and bilateral, symmetric impregnation of silver of the walls of the upper and middle regions of the nasal mucosa have been reported (Montaudon, 1959).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Seizures may be seen after oral ingestions (ITI, 1985).
    B) DIZZINESS
    1) WITH POISONING/EXPOSURE
    a) Dizziness may be seen after oral ingestions (ITI, 1985).
    C) NEUROPATHY
    1) WITH THERAPEUTIC USE
    a) SILVER DEPOSITION: Silver nitrate has previously been thought not to deposit silver in the CNS. However, animal studies have indicated that exogenous silver accumulates in neurons and protoplasmic glia cells of the brain and spinal cord.
    2) WITH POISONING/EXPOSURE
    a) SILVER DEPOSITION: Silver nitrate has previously been thought not to deposit silver in the CNS. However, animal studies have indicated that exogenous silver accumulates in neurons and protoplasmic glia cells of the brain and spinal cord.
    3) ANIMAL STUDIES: A 1985 study in rats showed that exogenous silver accumulates in neurons and protoplasmic glia cells of the brain and spinal cord (Rungby et al, 1985).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH THERAPEUTIC USE
    a) A burning sensation in the mouth may occur. Hemorrhagic, erosive intestinal lesions may occur (Marshall & Schneider, 1977). Vomitus may be black (JEF Reynolds , 1988).
    2) WITH POISONING/EXPOSURE
    a) Nausea, vomiting, and abdominal pain, as well as diarrhea may occur after ingestion (ITI, 1985; Rauber & Bruner, 1987). Abdominal pain may be violent (Stokinger, 1981).
    b) CASE REPORT: Vomiting occurred immediately following accidental ingestion of 60 mL and 16 mL of 24% silver nitrate solution in two pediatric patients. No burns were noted on subsequent physical examinations (Rauber & Bruner, 1987).
    B) DUODENITIS
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: In one unusual case, duodenal damage occurred in a 10-year-old child given a silver nitrate bladder instillation for bladder bleeding post chemotherapy. Some of the solution refluxed from the bladder to the kidney, extravasated from there, and damaged the duodenum (Anon, 1990).
    C) ESOPHAGITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Esophageal damage, including severe destruction of the mucosa with extensive deposits of clumps of brown pigment and edema of the remaining wall, was reported in a 40-year-old who swallowed silver salt with suicidal intent (Uhde, 1945).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) TOXIC NEPHROPATHY
    1) WITH THERAPEUTIC USE
    a) There may be silver deposits in the basement membrane of the kidney.
    1) There is still some controversy over whether this condition has any clinical significance.

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) METHEMOGLOBINEMIA
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: Methemoglobinemia developed in a 12-month-old female infant after being treated with a 0.5% silver nitrate solution for a complicated wound infection on her trunk. Approximately 20 days after the initiation of therapy, she was noted to be fussy, dyspneic and cyanotic. Her methemoglobin level was 38% (normal, less than 1%). She was treated with methylene blue (10 mg; 1 mg/kg) and recovered completely (Chou et al, 1999).
    b) CASE REPORT: Methemoglobinemia was noted in a 2-year-old girl treated with 0.5% silver nitrate solution for burns involving 50% of her body. After 11 days of treatment, her methemoglobin level was 59% (Strauch et al, 1969).
    c) CASE REPORTS: Methemoglobinemia has also been reported in 2 other burn patients, a 5-year-old and 3-year-old (Ternberg & Luce, 1968; Cushing & Smith, 1969). The most likely mechanism is conversion of nitrate to nitrite by organisms at the burn site.

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Silver nitrate is a skin irritant, and may cause dermatitis, rashes, or possibly burns (ITI, 1985).
    B) CHEMICAL BURN
    1) WITH THERAPEUTIC USE
    a) Infants treated with silver nitrate for umbilical granulomas have developed chemical burns (Chamberlain et al, 1992).
    C) DISCOLORATION OF SKIN
    1) WITH THERAPEUTIC USE
    a) Chronic ingestions of small quantities of silver nitrate or chronic exposures to this compound dermally may cause argyria.
    b) Argyria is an unsightly blue-gray discoloration of the skin, mucous membranes, and eyes due to silver accumulation. It may occur after exposure to silver nitrate (Shelley et al, 1987).
    c) This condition may mimic other clinical conditions such as cyanosis, methemoglobinemia, metastatic melanoma with metanogenuria, and hemochromatosis (Marshall & Schneider, 1977; Tanner & Gross, 1990).
    d) There are no associated physiological disturbances of the skin which are due to the silver deposition (Tanner & Gross, 1990).
    e) CASE REPORT: A 33-year-old woman had her tongue painted repeatedly for one year with 10% silver nitrate for the treatment of oral ulcers. Six years later she presented with darkening of her skin on her face, dorsa of hands and arms, sclera, conjunctiva, tongue, and oral mucous membranes. The darkening was due to argyria (Lee & Lee, 1994).
    2) WITH POISONING/EXPOSURE
    a) Chronic ingestions of small quantities of silver nitrate or chronic exposures to this compound dermally may cause argyria.
    b) Argyria is an unsightly blue-gray discoloration of the skin, mucous membranes, and eyes due to silver accumulation. It may occur after exposure to silver nitrate (Shelley et al, 1987).
    c) This condition may mimic other clinical conditions such as cyanosis, methemoglobinemia, metastatic melanoma with metanogenuria, and hemochromatosis (Marshall & Schneider, 1977; Tanner & Gross, 1990).
    d) There are no associated physiological disturbances of the skin which are due to the silver deposition (Tanner & Gross, 1990).
    D) CONTACT DERMATITIS
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: A 58-year-old patient undergoing patch testing for allergies had an unusual edge effect around an area marked with silver nitrate. Silver nitrate has been used to mark patch test sites, which in this case became the sensitizer (Iliev & Elsner, 1998).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7761-88-8 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor urea and electrolytes in symptomatic patients.
    B) Monitor methemoglobin levels in patients with symptoms of systemic absorption of silver nitrate or the presence of cyanosis.
    C) Following ingestion or suspected oral exposure to silver nitrate, endoscopy may be considered to rule out caustic injury.
    D) Obtain a baseline chest x-ray in a patient experiencing respiratory difficulties following an inhalation exposure.
    E) Obtain an ophthalmologic examination in patients with ocular symptoms after exposure to silver nitrate. It can also be used to detect exposure to silver nitrate as seen by deposits of silver in the eye by slit-lamp examination.
    F) Background serum levels of silver vary considerably but range from 0.04 mcg/g of blood to 0.3 mcg/g.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Background serum levels of silver vary considerably, ranging from 0.04 mcg/g blood to 0.3 mcg/g (Stokinger, 1981).
    4.1.4) OTHER
    A) OTHER
    1) Obtain an ophthalmologic examination in patients with ocular symptoms after exposure to silver nitrate. It can also be used to detect exposure to silver nitrate as seen by deposits of silver in the eye by slit-lamp examination (Humphreys & Routledge, 1998).

Methods

    A) SPECTROSCOPY/SPECTROMETRY
    1) Many methods exist to analyze silver. The two most common methods used for biologic samples are emission spectrochemical and atomic spectrophotometry (Stokinger, 1981).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Symptomatic patients, and those with endoscopically demonstrated grade II or higher burns should be admitted. Patients with evidence of respiratory distress, seizures, gastrointestinal bleeding, or large ingestions should be admitted to an intensive care setting.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with an ingestion or a suspected ingestion of silver nitrate should be sent to a health care facility for evaluation. Patients with an endoscopic evaluation that demonstrates no burns or only a minor grade I burn(s), and who can tolerate oral intake can be discharged home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a hospital intensivist in patients requiring intensive care admission. Consult an ophthalmologist for patients with persistent ocular symptoms following irrigation.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with a deliberate acute ingestion should be monitored for signs and symptoms of caustic injury. Endoscopy should be performed as necessary.

Monitoring

    A) Monitor urea and electrolytes in symptomatic patients.
    B) Monitor methemoglobin levels in patients with symptoms of systemic absorption of silver nitrate or the presence of cyanosis.
    C) Following ingestion or suspected oral exposure to silver nitrate, endoscopy may be considered to rule out caustic injury.
    D) Obtain a baseline chest x-ray in a patient experiencing respiratory difficulties following an inhalation exposure.
    E) Obtain an ophthalmologic examination in patients with ocular symptoms after exposure to silver nitrate. It can also be used to detect exposure to silver nitrate as seen by deposits of silver in the eye by slit-lamp examination.
    F) Background serum levels of silver vary considerably but range from 0.04 mcg/g of blood to 0.3 mcg/g.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Esophagoscopy may be indicated due to the caustic nature of silver nitrate. In this setting, activated charcoal may obscure endoscopy findings. Activated charcoal is NOT recommended in patients in whom significant gastrointestinal burns are likely (eg, presence of oral burns, persistent vomiting, drooling or stridor after ingestion).
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Silver nitrate may be caustic. Esophagoscopy may be indicated due to the caustic nature of this agent. Activated charcoal may obscure endoscopy findings. Activated charcoal is not recommended in patients in whom significant gastrointestinal burns are likely (ie, presence of oral burns, persistent vomiting, drooling or stridor after ingestion).
    a) The decision on esophagoscopy must be made on an individual case basis depending on factors such as the patient's symptoms, the concentration of the silver nitrate, and time it is left on the tissue.
    B) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    C) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive. Monitor vital signs. INGESTION: Perform oral exam to assess for mucous membrane injury. A minor "taste" ingestions of silver nitrate may only require dilution. If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting. Nausea and vomiting may develop following ingestion; monitor fluid status. Consider an endoscopy for a significant or suspected ingestion to assess for caustic injury. DERMAL: Remove contaminated clothing and copiously wash area with soap and water. Monitor electrolytes and/or methemoglobin level in patients with evidence of systemic injury. OCULAR: Copious irrigation; perform slit lamp exam. Consider Ophthalmology consult for persistent symptoms. ARGYRIA: If argyria develops, there is no effective treatment. Chelation therapy has not been found to be effective.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment is symptomatic and supportive. INGESTION: Endoscopy should be performed as needed in any patient with a silver nitrate ingestion and evidence of caustic injury. Early airway management in patients with upper airway edema or respiratory distress. SEIZURES: Treat seizures with IV benzodiazepines, barbiturates. METHEMOGLOBINEMIA: Determine the methemoglobin concentration. Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations). Administer oxygen while preparing for methylene blue therapy.
    B) MONITORING OF PATIENT
    1) Monitor urea and electrolytes in symptomatic patients.
    2) Monitor methemoglobin levels in patients with symptoms of systemic absorption of silver nitrate or the presence of cyanosis.
    3) Following ingestion or suspected oral exposure to silver nitrate, endoscopy may be considered to rule out caustic injury.
    4) Obtain a baseline chest x-ray in a patient experiencing respiratory difficulties following an inhalation exposure.
    5) Obtain an ophthalmologic examination in patients with ocular symptoms after exposure to silver nitrate. It can also be used to detect exposure to silver nitrate as seen by deposits of silver in the eye by slit-lamp examination.
    6) Many methods exist to analyze silver; background serum levels of silver vary considerably but range from 0.04 mcg/g of blood to 0.3 mcg/g. Urine, serum and hair can be tested for silver.
    C) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    D) ENDOSCOPIC PROCEDURE
    1) Silver nitrate may be caustic. There is little information regarding the use of endoscopy, corticosteroids or surgery in the setting of concentrated silver nitrate 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.
    a) REFERENCES: (Dogan et al, 2006; Symbas et al, 1983; Crain et al, 1984a; Gaudreault et al, 1983a; Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989; Previtera et al, 1990; Zargar et al, 1991; Vergauwen et al, 1991; Gorman et al, 1992)
    5) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):
    a) Advancing across the cricopharynx under direct vision
    b) Gently advancing with minimal air insufflation
    c) Never retroverting or retroflexing the endoscope
    d) Using a pediatric flexible endoscope
    e) Using extreme caution in advancing beyond burn lesion areas
    f) Most authors recommend endoscopy within the first 24 hours of injury, not advancing the endoscope beyond areas of severe esophageal burns, and avoiding endoscopy during the subacute phase of healing when tissue slough increases the risk of perforation (5 to 15 days after ingestion) (Zargar et al, 1991).
    6) GRADING
    a) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding, and perforation is related to the severity of the initial burn (Zargar et al, 1991):
    b) Grade 0 - Normal examination
    c) Grade 1 - Edema and hyperemia of the mucosa; strictures unlikely.
    d) Grade 2A - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely.
    e) Grade 2B - Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
    f) Grade 3A - Multiple ulcerations and small scattered areas of necrosis; strictures are common, complications such as perforation, fistula formation or gastrointestinal bleeding may occur.
    g) Grade 3B - Extensive necrosis through visceral wall; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding are more likely than with 3A.
    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).
    E) CORTICOSTEROID
    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
    a) ANIMAL
    1) Some animal studies have suggested that corticosteroid therapy may reduce the incidence of stricture formation after severe alkaline corrosive injury (Haller & Bachman, 1964; Saedi et al, 1973a).
    2) Animals treated with steroids and antibiotics appear to do better than animals treated with steroids alone (Haller & Bachman, 1964).
    3) Other studies have shown no evidence of reduced stricture formation in steroid treated animals (Reyes et al, 1974). An increased rate of esophageal perforation related to steroid treatment has been found in animal studies (Knox et al, 1967).
    b) HUMAN
    1) Most human studies have been retrospective and/or uncontrolled and generally involve small numbers of patients with documented second or third degree mucosal injury. No study has proven a reduced incidence of stricture formation from steroid use in human caustic ingestions (Haller et al, 1971; Hawkins et al, 1980; Yarington & Heatly, 1963; Adam & Brick, 1982).
    2) META ANALYSIS
    a) Howell et al (1992), analyzed reports concerning 361 patients with corrosive esophageal injury published in the English language literature since 1956 (10 retrospective and 3 prospective studies). No patients with first degree burns developed strictures. Of 228 patients with second or third degree burns treated with corticosteroids and antibiotics, 54 (24%) developed strictures. Of 25 patients with similar burn severity treated without steroids or antibiotics, 13 (52%) developed strictures (Howell et al, 1992).
    b) Another meta-analysis of 10 studies found that in patients with second degree esophageal burns from caustics, the overall rate of stricture formation was 14.8% in patients who received corticosteroids compared with 36% in patients who did not receive corticosteroids (LoVecchio et al, 1996).
    c) Another study combined results of 10 papers evaluating therapy for corrosive esophageal injury in humans published between January 1991 and June 2004. There were a total of 572 patients, all patients received corticosteroids in 6 studies, in 2 studies no patients received steroids, and in 2 studies, treatment with and without corticosteroids was compared. Of 109 patients with grade 2 esophageal burns who were treated with corticosteroids, 15 (13.8%) developed strictures, compared with 2 of 32 (6.3%) patients with second degree burns who did not receive steroids (Pelclova & Navratil, 2005).
    3) Smaller studies have questioned the value of steroids (Ferguson et al, 1989; Anderson et al, 1990), thus they should be used with caution.
    4) Ferguson et al (1989) retrospectively compared 10 patients who did not receive antibiotics or steroids with 31 patients who received both antibiotics and steroids in a study of caustic ingestion and found no difference in the incidence of esophageal stricture between the two groups (Ferguson et al, 1989).
    5) A randomized, controlled, prospective clinical trial involving 60 children with lye or acid induced esophageal injury did not find an effect of corticosteroids on the incidence of stricture formation (Anderson et al, 1990).
    a) These 60 children were among 131 patients who were managed and followed-up for ingestion of caustic material from 1971 through 1988; 88% of them were between 1 and 3 years old (Anderson et al, 1990).
    b) All patients underwent rigid esophagoscopy after being randomized to receive either no steroids or a course consisting initially of intravenous prednisolone (2 milligrams/kilogram per day) followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks prior to tapering and discontinuation (Anderson et al, 1990).
    c) Six (19%), 15 (48%), and 10 (32%) of those in the treatment group had first, second and third degree esophageal burns, respectively. In contrast, 13 (45%), 5 (17%), and 11 (38%) of the control group had the same levels of injury (Anderson et al, 1990).
    d) Ten (32%) of those receiving steroids and 11 (38%) of the control group developed strictures. Four (13%) of those receiving steroids and 7 (24%) of the control group required esophageal replacement. All but 1 of the 21 children who developed strictures had severe circumferential burns on initial esophagoscopy (Anderson et al, 1990).
    e) Because of the small numbers of patients in this study, it lacked the power to reliably detect meaningful differences in outcome between the treatment groups (Anderson et al, 1990).
    6) ADVERSE EFFECTS
    a) The use of corticosteroids in the treatment of caustic ingestion in humans has been associated with gastric perforation (Cleveland et al, 1963) and fatal pulmonary embolism (Aceto et al, 1970).
    F) SURGICAL PROCEDURE
    1) In severe cases of gastrointestinal necrosis or perforation, emergent surgical consultation should be obtained. The need for gastric resection or laparotomy in the stable patient is controversial (Chodak & Passaro, 1978; Dilawari et al, 1984).
    2) LAPAROTOMY/LAPAROSCOPY - Early laparotomy or laparoscopy should be considered in patients with endoscopic evidence of severe esophageal or gastric burns after acid ingestion to evaluate for the presence of transmural gastric or esophageal necrosis (Estrera et al, 1986; Meredith et al, 1988; Wu & Lai, 1993). Emergent laparotomy should be strongly considered in any patient with hypotension, altered mental status, or acidemia (Hovarth et al, 1991).
    a) STUDY - In a retrospective study of patients with extensive transmural gastroesophageal necrosis after caustic ingestion, all 4 patients treated in the conventional manner (endoscopy, steroids, antibiotics, and repeated evaluation for the occurrence of esophagogastric necrosis and perforation) died, while all 3 patients treated with early laparotomy and immediate esophagogastric resection survived (Estrera et al, 1986).
    b) Wu & Lai (1993) reported the results of emergency surgical resection of the alimentary tract in 28 patients who had extensive corrosive injuries due to the ingestion of acids or other caustics. Operative mortality was most frequently associated with sepsis. Non-fatal bleeding, infections, biliary or bronchial fistulas were other noted complications. Morbidity and mortality were related to the severity of the damage and the extent of surgery required.
    1) Immediate postoperative management included antibiotics, extensive respiratory care, tracheobronchial toilet, maintenance of fluid, electrolyte and acid-base balance, and jejunostomy feeding or total parenteral nutrition.
    G) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    H) METHEMOGLOBINEMIA
    1) SUMMARY
    a) Determine the methemoglobin concentration and evaluate the patient for clinical effects of methemoglobinemia (ie, dyspnea, headache, fatigue, CNS depression, tachycardia, metabolic acidosis). Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations in patients with anemia, or underlying pulmonary or cardiovascular disorders). Administer oxygen while preparing for methylene blue therapy.
    2) METHYLENE BLUE
    a) 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 (Prod Info PROVAYBLUE(TM) intravenous injection, 2016) and 10 mg/1 mL (1% solution) vials (Prod Info methylene blue 1% intravenous injection, 2011). REPEAT DOSES: Additional doses may be required, especially for substances with prolonged absorption, slow elimination, or those that form metabolites that produce methemoglobin. NOTE: Large doses of methylene blue may cause methemoglobinemia or hemolysis (Howland, 2006). 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 (Prod Info methylene blue 1% intravenous injection, 2011; Herman et al, 1999). NEONATES: DOSE: 0.3 to 1 mg/kg (Hjelt et al, 1995).
    b) CONTRAINDICATIONS: G-6-PD deficiency (methylene blue may cause hemolysis), known hypersensitivity to methylene blue, methemoglobin reductase deficiency (Shepherd & Keyes, 2004)
    c) FAILURE: Failure of methylene blue therapy suggests: inadequate dose of methylene blue, inadequate decontamination, NADPH dependent methemoglobin reductase deficiency, hemoglobin M disease, sulfhemoglobinemia, or G-6-PD deficiency. Methylene blue is reduced by methemoglobin reductase and nicotinamide adenosine dinucleotide phosphate (NADPH) to leukomethylene blue. This in turn reduces methemoglobin. Red blood cells of patients with G-6-PD deficiency do not produce enough NADPH to convert methylene blue to leukomethylene blue (do Nascimento et al, 2008).
    d) DRUG INTERACTION: Concomitant use of methylene blue with serotonergic drugs, including serotonin reuptake inhibitors (SRIs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), norepinephrine-dopamine reuptake inhibitors (NDRIs), triptans, and ergot alkaloids may increase the risk of potentially fatal serotonin syndrome (U.S. Food and Drug Administration, 2011; Stanford et al, 2010; Prod Info methylene blue 1% IV injection, 2011).
    3) TOLUIDINE BLUE OR TOLONIUM CHLORIDE (GERMANY)
    a) DOSE: 2 to 4 mg/kg intravenously over 5 minutes. Dose may be repeated in 30 minutes (Nemec, 2011; Lindenmann et al, 2006; Kiese et al, 1972).
    b) SIDE EFFECTS: Hypotension with rapid intravenous administration. Vomiting, diarrhea, excessive sweating, hypotension, dysrhythmias, hemolysis, agranulocytosis and acute renal insufficiency after overdose (Dunipace et al, 1992; Hix & Wilson, 1987; Winek et al, 1969; Teunis et al, 1970; Marquez & Todd, 1959).
    c) CONTRAINDICATIONS: G-6-PD deficiency; may cause hemolysis.
    I) ARGYRIA OF SKIN
    1) HYDROQUINONE: It has been reported that treatment with 5% hydroquinone could reduce the number of silver granules in the upper dermis and surrounding sweat glands and reduce the number of melanocytes (which are reportedly increased in argyria) (Lee & Lee, 1994; Lai-Becker & Ewald, 2011).
    a) There has been some success with hydroquinone (5%), but additional studies are suggested (Bleehen et al, 1981).
    2) LASER THERAPY: Successful use of this therapy has been reported to treat argyria (Lai-Becker & Ewald, 2011).
    3) SELENIUM AND SULFUR: These agents have been considered for the treatment of argyria. Selenium may act to precipitate or chelate silver; it is theorized that an increase in selenium intake can bind with silver for excretion rather than being deposited in the skin. Silver sulfur complexes have also be evaluated for similar effects, although it is not as stable (Lai-Becker & Ewald, 2011).
    4) OTHER THERAPIES: Local injections of 6% sodium thiosulfate and 1% potassium ferrocyanide have been tried to decrease silver concentrations in small areas, but have NOT been particularly effective and have produced a moderate amount of pain (Marshall & Schneider, 1977).
    J) CHELATION THERAPY
    1) SUMMARY
    a) Chelation, such as that done with lead, has NOT been successful (Aub & Fairhall, 1942). Silver deposited in the tissues is relatively inert and difficult to chelate (Aaseth et al, 1981; Lai-Becker & Ewald, 2011).
    2) BAL
    a) BAL has NOT been found to be effective because elemental silver deposits are difficult to chelate. Historically, BAL was thought to be a chelator of choice (Bessman & Doorenbos, 1957); however most texts list it as NOT effective.
    3) D-PENICILLAMINE AND N-ACETYL-DL-PENICILLAMINE
    a) These agents did NOT increase the excretion of silver in argyria. Although the silver-albuminate complex does release 20 to 25% of the silver to penicillamine in vitro, this is not seen in vivo (Aaseth et al, 1981).
    4) DIMERCAPTOPROPANE SULFONATE/DMPS
    a) A 60-year-old man with argyria from use of 30 mL of 3% silver nitrate solution for treatment of gingival erosions from ill fitting dentures was chelated with DMPS 0.5 to 2.5 grams/day for two 5-day periods.
    1) Maximal urinary excretion values of 50 nanomoles/day were reported. The authors estimated the total amount of urinary excreted silver during 10 days of chelation to be 0.35 micromoles. The amount excreted by this chelator is only 0.0066 percent of the estimated body burden (5.3 millimoles). It was concluded that DMPS was NOT an effective chelator of silver (Aaseth et al, 1986).
    5) ETHYLENEDIAMINE
    a) Ethylenediamine has NOT been found to be effective because the elemental silver deposits are difficult to chelate (Marshall & Schneider, 1977).
    K) EXPERIMENTAL THERAPY
    1) SODIUM CHLORIDE
    a) Some authors recommend a 1% solution of sodium chloride to be given orally to precipitate silver chloride and prevent systemic chloride depletion (JEF Reynolds , 1988).
    b) This treatment has NOT been consistently effective and cannot be recommended routinely.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Silver nitrate is a strong irritant, and if inhaled in sufficient quantities may cause pulmonary irritation, cough, and bronchitis.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: 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, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    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).

Abstracts

Case Reports

    A) ADVERSE EFFECTS
    1) Two patients seen in the same emergency room were administered 60 mL and 16 mL from a stock bottle labeled sodium sulfate 20%. Each vomited immediately. Both were sent home. One child returned the next day with a dark stain of the area where vomitus had contacted the skin on the previous day. The stock bottle was analyzed and found to be silver nitrate 24%. No burns to either child were noted on subsequent physical exams (Rauber & Bruner, 1987).

Range Of Toxicity

Summary

    A) TOXICITY: ACUTE TOXICITY: The estimated acute oral fatal dose is approximately 10 g (form not specified) but 30 g has been survived. Silver nitrate is a strong irritant and would be expected to cause strong irritation or burns on skin and mucous membranes. ARGYRIA: On the average, argyria occurs after administration of 1 g of elemental silver by injection or 3.8 g of orally administered silver. METHEMOGLOBINEMIA: The most likely mechanism is conversion of nitrate to nitrite by organisms at the burn site resulting in methemoglobinemia in some patients. In severe cases, it may lead also lead to cyanosis and death.

Minimum Lethal Exposure

    A) ACUTE
    1) Silver nitrate is a strong irritant, and would be expected to cause strong irritation or burns on skin and mucous membranes.
    2) The estimated acute oral fatal dose is approximately 10 g (form not specified) but 30 g has been survived (Stokinger, 1981; Sollman, 1957).

Maximum Tolerated Exposure

    A) ARGYRIA
    1) Argyria may occur due to exposure to silver nitrate. Cases of argyria have not resulted from silver concentrations in air less than 0.01 mg/cubic meter (ACGIH, 1980).
    2) On the average, argyria occurs after administration of 1 g of elemental silver by injection and 3.8 g of orally administered silver (ACGIH, 1980).
    B) METHEMOGLOBINEMIA
    1) MECHANISM: The most likely mechanism is conversion of nitrate to nitrite by organisms at the burn site resulting in methemoglobinemia in some patients. In severe cases, it may lead also lead to cyanosis and death (Humphreys & Routledge, 1998).
    2) CASE REPORT: Methemoglobinemia was noted in a 2-year-old girl treated with 0.5% silver nitrate solution for burns involving 50% of her body. After 11 days of treatment, her methemoglobin level was 59% (Strauch et al, 1969).
    3) CASE REPORTS: Methemoglobinemia has also been reported in 2 other burn patients, a 5-year-old and 3-year-old (Ternberg & Luce, 1968; Cushing & Smith, 1969).
    C) CASE REPORTS
    1) PEDIATRIC
    a) Two pediatric patients accidently ingested 60 and 16 mL of 24% silver nitrate, respectively, and vomited immediately. No burns were observed in either child following physical examination (Rauber & Bruner, 1987).

Workplace Standards

    A) ACGIH TLV Values for CAS7761-88-8 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS7761-88-8 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS7761-88-8 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS7761-88-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (INTRAPERITONEAL)MOUSE:
    1) 129 mcg/kg (ITI, 1985)
    B) LD50- (ORAL)MOUSE:
    1) 50 mg/kg (ITI, 1985)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Silver nitrate in concentrations between 0.5% and 1% are used as antibacterial agents (Block et al, 1974).
    B) Concentrations of silver nitrate greater than 1% have astringent, irritant, or caustic properties (JEF Reynolds , 1988).

Toxicologic Mechanism

    A) Systemic silver toxicity rarely occurs beyond argyria due to rapid binding to various proteins and precipitation of silver chloride. Tissue damage occurs only when this binding ability is overwhelmed by a massive dose.
    1) Slow administration allows more binding time and distribution, therefore less tissue damage (Marshall & Schneider, 1977).
    B) Silver nitrate is also a strong caustic and will cause tissue damage and necrosis.

Physicochemical

Physical Characteristics

    A) Silver nitrate is a colorless, odorless, crystal with a metallic taste (ITI, 1985).

Ph

    A) 5.4-6.4 (4% solution) (Windholz, 1983)
    B) A 2.7% solution is iso-osmotic with serum (JEF Reynolds , 1988).

Molecular Weight

    A) 169.87 (Stokinger, 1981)

Other

    A) ODOR THRESHOLD
    1) Odorless (CHRIS , 2002)

References

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