Tox: Industrial toxins

Question 1

Sources of hydrogen fluoride

Answer 1

Rust removers, oven cleaners, automotive wheel cleaners.

Commercial sources: glass etching, graffiti removal, manufacture of certain fuels

Question 2

Mxn of HF toxicity

Answer 2

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.

Question 3

Symptoms/exam findings with HF toxicity

Answer 3

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).

Question 4

Tx of local HF toxicity

Answer 4

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.

Question 5

Tx of large dermal or systemic HF exposure

Answer 5

Obtain central access, provide aggressive empiric calcium repletion.

Question 6

Is most lead toxicity due to acute or chronic exposures?

Answer 6

Most lead toxicity is due to chronic, low level exposure. Acute toxicity from single exposure is rare.

Question 7

Sources of lead exposure

Answer 7

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)

Question 8

Mxn of lead toxicity

Answer 8

Inhibits wide variety of cellular enzymes, reduces ability to synthesize heme, directly damages peripheral nerves.

Question 9

Signs/symptoms lead toxicity

Answer 9

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.

Question 10

Diagnosis of lead toxicity

Answer 10

Direct measurement of lead in whole blood.
Look for basophilic stippling anemia.
Lead-containing material usually visible on XR if ingested.

Question 11

Tx of lead poisoning

Answer 11

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.

Question 12

Sources of arsenic

Answer 12

Pesticides, wood preservatives, metal alloys, chemical synthesis, glass manufacturing, folk remedies

Question 13

Mxn of arsenic toxicity

Answer 13

Inhibits key enzymes in cellular oxidative metabolism.

Causes acute hemolysis.

Question 14

Symptoms of chronic arsenic poisoning

Answer 14

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.

Question 15

Symptoms of acute arsenic poisoning

Answer 15

Mainly GI: violent rice water gastritis. 
Confusion, coma, seizures. 
HypoTN, +HR, prolonged QTc, torsades. 
ARDS. 
Symptoms may be delayed 2-24hrs.

Question 16

Diagnosis of arsenic poisoning

Answer 16

Suspect based on clinical presentation/possible exposure.

24hr urine arsenic level (may be falsely elevated after consumption of seafood).

Question 17

Tx of arsenic poisoning

Answer 17

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.

Question 18

3 forms of mercury

Answer 18

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.

Question 19

Symptoms of acute mercury inhalation (quicksilver)

Answer 19

Rapid onset SOB, cough, chills, fever, resp distress.

Question 20

Symptoms of chronic mercury poisoning (quicksilver inhalation- e.g. hat makers)

Answer 20

Tremor, neuropsychiatric disturbance (shyness, withdrawal, depression), gingivostomatitis, AN, sweating, acrodynia (pain to extremities), pink discoloration and desquamation of extremities.

Question 21

Symptoms of acute ingestion of mercury salts

Answer 21

Corrosive gastroenteritis w/ shock, ARF, grayish discoloration of mucus membranes and metallic taste.

Question 22

Symptoms of acute ingestion of organic mercury

Answer 22

Delayed permanent neurotoxicity- ataxia, dysarthria, constricted visual fields

Question 23

Treatment of mercury poisoning

Answer 23

WBI if radiopaque objects visible on XR.

Antidote = BAL if severe GI symptoms or DMSA if able to tolerate PO