Tox: Industrial toxins Flashcards
Sources of hydrogen fluoride
Rust removers, oven cleaners, automotive wheel cleaners.
Commercial sources: glass etching, graffiti removal, manufacture of certain fuels
Mxn of HF toxicity
Absorbed by skin/MM –> deep penetration and cellular destruction –> +++pain.
Highly reactive fluoride ion binds extracellular Mg/Ca –> hypocalcemia, hypomagnesemia.
Systemic hypocalcemia/hypomag may occur with ingestion or heavy dermal exposure.
Delayed onset hyperK due to cellular breakdown, acidosis, direct fluoride effects on K efflux.
Symptoms/exam findings with HF toxicity
Direct relationship between [HF] and time to symptom onset:
- > 10% sol = earlier onset
- Onset can be delayed up to 24hrs if dilute.
Dermal exposure/low conc: local pain, erythema, swelling, white-blue discoloration (esp subungual/under nails).
- pain out of proportion to skin findings.
If oral ingestion or large dermal exposure: systemic hypocalcemia (tetany, weakness, Chvostek sign, life threatening dysrhythmia, sudden death).
Tx of local HF toxicity
Calcium gluconate should be given as:
- Topical paste
- SQ and intradermal ingestions (caution in digits)
- Nebulized if inhalational exposure.
- Regional intra-arterial infusion
Can do Bier block.
Tx of large dermal or systemic HF exposure
Obtain central access, provide aggressive empiric calcium repletion.
Is most lead toxicity due to acute or chronic exposures?
Most lead toxicity is due to chronic, low level exposure. Acute toxicity from single exposure is rare.
Sources of lead exposure
Adults: primarily occupational (construction, mining, welding, smelting, manufacture of batteries, plastics, rubber, moonshine).
Pediatric: typically accidental ingestion of lead-containing materials (paint chips, imported toys, jewelry)
Mxn of lead toxicity
Inhibits wide variety of cellular enzymes, reduces ability to synthesize heme, directly damages peripheral nerves.
Signs/symptoms lead toxicity
Most common: subtle neurological changes, anemia, HTN.
Chronic: subtle, insidious, nonspecific symptoms. HA, peripheral motor neuropathy (wrist drop), HTN, anemia, gout, cognitive impairment.
Acute: n/v, constipation, abdominal pain (lead colic), anemia, encephalopathy, ataxia, seizures.
Diagnosis of lead toxicity
Direct measurement of lead in whole blood.
Look for basophilic stippling anemia.
Lead-containing material usually visible on XR if ingested.
Tx of lead poisoning
AC does NOT bind. WBI if visible material on XR. Chelation: - BAL (british anti-lewisite, dimercaprol) and Ca-EDTA for severely poisoned patients (symptomatic w/ encephalopathy or level >100 mcg/dL) - Tx w/ BAL first then with Ca-EDTA
Alternative chelator: DMSA.
Oral chelation therapy if no acute symptoms and child with lead level >45 mcg/dL or level >80mcg/dL in asymptomatic adult.
Sources of arsenic
Pesticides, wood preservatives, metal alloys, chemical synthesis, glass manufacturing, folk remedies
Mxn of arsenic toxicity
Inhibits key enzymes in cellular oxidative metabolism.
Causes acute hemolysis.
Symptoms of chronic arsenic poisoning
Peripheral neuropathy, HA, ataxia, confusion, malaise.
Hyperpigmentation, Mees lines (transverse white lines on nails- appear weeks/mo after exposure), alopecia.
Hyperkeratotic lesions to palms, soles.
Cancers -> skin, bladder, lung.
Symptoms of acute arsenic poisoning
Mainly GI: violent rice water gastritis. Confusion, coma, seizures. HypoTN, +HR, prolonged QTc, torsades. ARDS. Symptoms may be delayed 2-24hrs.
Diagnosis of arsenic poisoning
Suspect based on clinical presentation/possible exposure.
24hr urine arsenic level (may be falsely elevated after consumption of seafood).
Tx of arsenic poisoning
WBI if radio-opaque objects on XR.
Antidote: BAL for chelation if severe GI symptoms.
DMSA in chronic poisoning and in acute poisonings once hemodynamically stable and GI symptoms resolved.
3 forms of mercury
1) Elemental mercury (quicksilver): e.g. in mercury containing devices in workplace or home such as thermometer.
2) Inorganic mercury salts: e.g. calomel in skin lightening creams.
3) Organic mercury: occupational/agricultural sources.
Symptoms of acute mercury inhalation (quicksilver)
Rapid onset SOB, cough, chills, fever, resp distress.
Symptoms of chronic mercury poisoning (quicksilver inhalation- e.g. hat makers)
Tremor, neuropsychiatric disturbance (shyness, withdrawal, depression), gingivostomatitis, AN, sweating, acrodynia (pain to extremities), pink discoloration and desquamation of extremities.
Symptoms of acute ingestion of mercury salts
Corrosive gastroenteritis w/ shock, ARF, grayish discoloration of mucus membranes and metallic taste.
Symptoms of acute ingestion of organic mercury
Delayed permanent neurotoxicity- ataxia, dysarthria, constricted visual fields
Treatment of mercury poisoning
WBI if radiopaque objects visible on XR.
Antidote = BAL if severe GI symptoms or DMSA if able to tolerate PO
