Patient's question:
Hello: While measuring temperature, I bit and broke the thermometer, swallowed half of the mercury. Is there any way to get the mercury out? What are the effects on the baby if I become pregnant in the future? Thank you!Doctor's answer:
Mercury is a silver-white liquid metal that evaporates at room temperature. Mercury poisoning (mercurypoisoig) is most commonly chronic, primarily occurring in production activities due to long-term inhalation of mercury vapor and mercury compound dust. The main symptoms include mental-neurological abnormalities, gingivitis, and tremors. Acute mercury poisoning occurs with the inhalation of high-dose mercury vapor or the ingestion of mercury compounds. Individuals allergic to mercury may experience poisoning even with local application of mercury oil-based preparations. Workers with frequent exposure to mercury include those involved in mercury mining, mercury alloy smelting, gold and silver extraction, mercury rectifiers, as well as production workers in vacuum pumps, lighting fixtures, instruments, thermometers, dental mercury alloys, fulminate of mercury, pigments, pharmaceuticals, nuclear reactor coolants, and atomic radiation protection materials. Organic mercury compounds were previously mainly used as agricultural disinfectants but are highly toxic, and their production and use have been discontinued in China.Diagnosis
The diagnosis of acute mercury poisoning is primarily based on occupational history or ingestion of toxic substances, combined with clinical manifestations and elevated urinary or blood mercury levels (significantly increased). The diagnosis of chronic mercury poisoning should emphasize exposure history, clinical symptoms such as mental-neurological manifestations, oral inflammation, and tremors, while ruling out similar clinical presentations caused by other etiologies. Elevated urinary and blood mercury levels are of diagnostic significance. Chelation tests can be performed using sodium dimercapto succinate (0.25g, intramuscular injection) or sodium dimercapto propyl succinate (0.5g, intravenous injection). A significantly increased excretion of urinary mercury can serve as an important diagnostic basis.
Treatment Measures
For acute poisoning caused by oral mercury compounds, gastric lavage should be performed immediately. Alternatively, raw egg white, milk, or activated charcoal may be administered orally; magnesium sulfate (50%) may be used for catharsis. During gastric lavage, the risk of perforation of the digestive tract must be monitored. Common antidotes for mercury include the following:
1. Sodium dimercapto succinate: Its thiol group binds with mercury ions to form a thiol-mercury complex, which is excreted in the urine, restoring enzyme activity inhibited by mercury ions. The initial dose for acute poisoning is a 5% solution (2–3ml, intramuscular injection), followed by 1–2.5ml every 4–6 hours. After 1–2 days, the dose is reduced to once daily (2.5ml). Treatment typically lasts about a week, with chelation possible again after one month if necessary. Common side effects include dizziness, headache, nausea, reduced appetite, and fatigue. Occasionally, abdominal pain or hypokalemia may occur, while a few patients may develop rashes, and rare cases of systemic allergic reactions or exfoliative dermatitis.
2. Sodium dimercaptoethanol: Its pharmacological effects are similar to sodium dimercapto succinate. The initial dose is 2.5–3.0mg/kg body weight, administered deep intramuscularly every 4–6 hours for 1–2 days. On the third day, the dosage is adjusted to every 6–12 hours, followed by once daily for 1–2 times. The total treatment duration is 10–14 days. Common side effects include headache, nausea, throat burning, tearing, nasal congestion, sweating, abdominal pain, muscle cramps, tachycardia, elevated blood pressure, rashes, and renal function impairment. Children are more prone to allergic reactions and fever.
3. Acetylcysteine (N-Acetyl-D,L-cysteine): It has lower renal toxicity than penicillamine and is taken orally in a daily dose of 1g, divided into four doses. Side effects include fatigue, dizziness, nausea, diarrhea, and urinary tract burning pain. A few patients may experience fever, rashes, lymphadenopathy, and leukopenia as allergic reactions.
During acute poisoning treatment, attention should be paid to maintaining water, electrolyte, and acid-base balance, as well as correcting shock. In cases of renal damage or acute renal failure, chelation drugs should be avoided, and blood dialysis or hemoperfusion should be initiated early. Chelation drugs may be used concurrently to reduce mercury toxicity.
For chronic mercury poisoning, chelation treatment involves intramuscular injection of 2.5–5.0ml of 5% sodium dimercapto succinate once daily for three consecutive days, followed by a four-day break, constituting one course. Generally, 2–3 courses are administered. Additionally, sodium dimercapto propyl succinate and penicillamine are also commonly used chelation drugs.
Pathogenesis
Mercury vapor readily penetrates the lipid-rich cell membranes of alveoli and binds with blood lipids, rapidly distributing to all tissues. In red blood cells and other tissues, mercury is oxidized to Hg2+ and binds with proteins, accumulating and being released with difficulty. Elemental mercury is poorly absorbed in the gastrointestinal tract, accounting for only about 0.001% of the ingested amount, while mercury salts are absorbed to a degree of about 10%. Mercury is primarily excreted through urine and feces, with small amounts excreted in saliva, milk, sweat, and minimal amounts through the lungs. The half-life of mercury in the body is 60 days for elemental mercury and 40 days for mercury salts, with higher excretion rates in the first four days. Mercury ions readily bind with thiol groups, inactivating enzymes such as cytochrome oxidase, pyruvate kinase, and succinate dehydrogenase. Mercury also binds with amino, carboxyl, and phosphoryl groups, affecting the activity of functional groups. Due to the impairment of these enzymes and functional groups, cellular bioactivity and normal metabolism are disrupted, ultimately leading to cell degeneration and necrosis.
In recent years, it has been discovered that mercury causes kidney damage, primarily affecting proximal tubular epithelial cells. Mercury can also induce immune dysfunction, leading to the production of autoantibodies and conditions such as nephrotic syndrome or glomerulonephritis.
Clinical Manifestations
1. Acute Mercury Poisoning
This is primarily caused by ingesting mercury compounds such as mercuric chloride. Symptoms appear within minutes to tens of minutes after ingestion, causing acute corrosive oral and gastrointestinal inflammation. Patients report oral and throat burning pain, accompanied by nausea, vomiting, abdominal pain, and diarrhea. Vomitus and feces often contain bloody mucus and necrotic tissue. Patients may also experience peripheral circulatory failure and gastrointestinal perforation. Acute renal failure may develop within 3–4 days (or within 24 hours in severe cases), accompanied by liver damage. Inhalation of high-concentration mercury vapor can cause fever, chemical tracheobronchitis, and pneumonia, leading to respiratory failure and acute renal failure. Skin contact with mercury and its compounds may cause contact dermatitis with allergic characteristics. The rash is erythematous papules, which may merge into patches or form vesicles, leaving hyperpigmentation after healing.
2. Chronic Mercury Poisoning
This is usually caused by occupational inhalation of mercury vapor, though a few cases may result from the use of mercury preparations. Mental-neurological symptoms may initially include dizziness, headache, insomnia, and dreams, followed by emotional disturbances such as agitation or depression, anxiety, timidity, and vegetative nervous system dysfunction (e.g., facial flushing, excessive sweating, skin scratch sign). Muscle tremors first appear in fingers, eyelids, and the tongue, then progress to arms, legs, and the head, and may even affect the entire body, becoming more pronounced under attention or excitement. Oral symptoms primarily include mucosal congestion, ulcers, gingival swelling and bleeding, loose or teeth. In individuals with poor oral hygiene, blue-black mercury sulfide particles may form linear "mercury lines" on the gums, marking mercury absorption. Renal involvement may initially present as subclinical tubular dysfunction (e.g., low-molecular-weight proteinuria) or progress to nephritis and nephrotic syndrome. Renal damage may recover after mercury exposure. Chronic poisoning patients may also experience weight loss, reduced sexual function, menstrual disorders or abortion in women, hyperthyroidism, and peripheral neuropathy. Brownish light reflex in the anterior chamber of the eye, considered "mercury cataractitis" caused by mercury deposition, may persist even after symptom resolution or mercury exposure, serving as another marker of mercury absorption.
Auxiliary Examinations
Urinary and blood mercury tests reflect, to some extent, the absorption of mercury in the body but often do not correlate with clinical symptoms or severity. Normal urinary mercury levels vary by region. In China, the upper limit for urinary mercury by the dithizone thermal nitration method is generally not exceeding 0.25μmol/L (0.05mg/L) or 0.1μmol/L (0.02mg/L) by atomic absorption spectrometry. The upper limit for blood mercury is 1.5μmol/L (0.03mg/dL). In chronic mercury poisoning, changes in EEG amplitude and electrical activity, slowed peripheral nerve conduction velocity, elevated blood α2-globulin and reduced glutathione, as well as decreased lysosomal enzymes, red blood cell cholinesterase, and serum thiol levels may be observed.