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 get 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 more commonly chronic and primarily occurs in production activities due to long-term inhalation of mercury vapor and dust from mercury compounds. 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 matrix 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 those producing vacuum pumps, lighting fixtures, instruments, thermometers, dental mercury alloys,, pigments, pharmaceuticals, nuclear reactor coolants, and atomic radiation protection materials. Organic mercury compounds were previously mainly used as agricultural fungicides 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 symptoms and elevated urinary or blood mercury levels (significantly increased). The diagnosis of chronic mercury poisoning should emphasize exposure history, clinical manifestations such as mental-neurological symptoms, oral inflammation, and tremors, while ruling out other causes of similar clinical presentations. 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
In cases of acute poisoning caused by oral mercury compounds, gastric lavage should be performed immediately. Alternatively, raw egg white, milk, or activated charcoal can be administered orally, followed by a cathartic using 50% magnesium sulfate. During gastric lavage, caution must be exercised to prevent perforation of the digestive tract. 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 function 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 2.5ml once daily for about one week. If necessary, chelation can be repeated after one month. Common side effects include dizziness, headache, nausea, reduced appetite, and fatigue. Occasionally, abdominal pain or hypokalemia may occur, while rare cases may present with rashes, systemic allergic reactions, or exfoliative dermatitis.
2. Dimercaprol: Its pharmacological effects are similar to sodium dimercapto succinate. The initial dose is 2.5–3.0mg/kg body weight, administered deeply intramuscularly every 4–6 hours for 1–2 days. On the third day, the frequency is adjusted based on the condition (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-peptidase): It has lower renal toxicity compared to penicillamine. The daily dose is 1g, taken four times orally. Side effects include fatigue, dizziness, nausea, diarrhea, and urinary tract burning pain. Some may experience fever, rashes, lymph node enlargement, and leukopenia.
During acute poisoning treatment, attention should be paid to maintaining water, electrolyte, and acid-base balance and correcting shock. In cases of renal damage or acute renal failure, chelating drugs should be avoided, and blood dialysis or hemoperfusion should be initiated early. Chelating drugs can be administered concurrently to reduce mercury toxicity.
For chronic mercury poisoning, chelation therapy 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 per course. Generally, 2–3 courses are administered. Additionally, sodium dimercapto propyl succinate and penicillamine are also commonly used chelating agents.
Prevention Measures
Mercury vapor adheres to surfaces and continuously evaporates at room temperature. Therefore, the walls, floors, and work surfaces in mercury-containing workshops should be smooth and free of cracks to facilitate cleaning and decontamination. The temperature in the workshop should not exceed 15–16°C. The maximum allowable concentration of mercury in the air of such workshops is set at 0.001mg/m3.
Pathogenesis
Mercury vapor easily 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 lesser extent (approximately 10%). Mercury is primarily excreted via urine and feces, with small amounts also excreted in saliva, milk, sweat, and exhaled air. 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.
Recent studies have shown that mercury causes kidney damage, primarily affecting proximal tubular epithelial cells. Mercury can also disrupt immune function, 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 ingestion of mercury compounds such as mercuric chloride. Symptoms appear within minutes to tens of minutes after ingestion, including acute corrosive oral and gastrointestinal inflammation. Patients report oral and throat burning pain, followed by nausea, vomiting, abdominal pain, and diarrhea. Vomitus and feces may contain bloody mucus and necrotic tissue. Peripheral circulatory failure and gastrointestinal perforation may occur. Acute renal failure can 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, pneumonia, respiratory failure, and acute renal failure. Skin contact with mercury and its compounds may lead to contact dermatitis with allergic characteristics. The rash appears as 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 some cases result from the use of mercury-containing preparations. Mental-neurological symptoms may initially include dizziness, headache, insomnia, and dreams, followed by emotional disturbances such as agitation, depression, anxiety, and timidity, as well as autonomic nervous system dysfunction (e.g., flushing, excessive sweating, skin scratch test positivity). Muscle tremors first appear in fingers, eyelids, and the tongue, then progress to arms, legs, and the head, and may become generalized, worsening with attention or excitement. Oral symptoms primarily include mucosal congestion, ulcers, gingival swelling and bleeding, loose or falling teeth. Poor oral hygiene may lead to the presence of blue-black mercury sulfide particles arranged in rows (mercury lines), indicating 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 cessation of mercury exposure. Chronic poisoning patients may also experience weight loss, reduced sexual function, menstrual disorders or miscarriage in women, hyperthyroidism, and peripheral neuropathy. Brownish light reflex in the anterior chamber of the eye, termed "mercury cataract," may persist even after symptom resolution or cessation of 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 using the dithizone thermal nitration method is generally not exceeding 0.25μmol/L (0.05mg/L) or 0.1μmol/L (0.02mg/L) using atomic absorption spectroscopy. 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 α?-globulin and reduced glutathione, as well as decreased lysosomal enzymes, red blood cell cholinesterase, and serum thiol levels may be observed.