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1. Heavy metal poisning

2. Introduction
These are inorganic elements that have a density greater than 5 g/ cm3 [1]. Examples of common
heavy metals are chromium (Cr), lead (Pb), cadmium (Cd), mercury (Hg), copper (Cu) and zinc
(Zn). Arsenic (As) is also included in this group because of similarities in physical and chemical
properties. Less common heavy metals include iron (Fe), cobalt (Co) and manganese (Mn). Heavy
metals were classified into two groups based on their toxicity, essential and non-essential heavy
metal. (1) Essential heavy metals are harmless or relatively less harmless at low concentration (Zn,
Cu, Fe, and Co). (2) Non-essential metals are highly toxic even at low concentration (such as Cd,
Hg, As, and Cr).

3. Mercury
Mercury poisoning remains an infrequently considered clinical
syndrome despite the fact that mercury is the second most common
cause of heavy metal poisoning.
Epidemiology and Environmental Sources Mercury ranks approximately 67th in
natural abundance among the elements in crustal rocks. It is found in the
environment in 3 major chemical states: elemental mercury or mercury vapor,
inorganic mercury or salts of mercury, and organic mercury or organomercurials
(eg, methyl, phenyl, alkyl). 13 Large quantities of mercury are released into the
atmosphere through several mechanisms including the degassing of the earth's
crust and oceans, which produces about 150,000 tons of mercury, and the
combustion of fossil fuels and other industrial activities, which adds another 20,000
tons. 19-22 An additional 10 tons of mercury are produced for industrial use
annually. 23 The main forms of mercury are discussed below; Table 1 summarizes
the most common sources of mercury exposure.

4. Symptoms of mercury poisoning Mercury is most notable for its neurological
effects. In general, the U.S.
Food and Drug Administration Trusted Source says that too much mercury can
cause:
anxiety
depression
Irritability
memory problems
numbness
pathologic shyness
tremors

5. Complications of mercury poisoning
High amounts of mercury can lead to long-term and sometimes
permanent neurological changes. The dangers are especially notable
in young children who are still developing.
Mercury exposure can lead to developmental problems in the brain,
which can also affect physical functions such as motor skills. Some
children who are exposed to mercury at a young age may develop
learning disabilities, according to the Environmental Defense Fund.
Adults with mercury poisoning may have permanent brain and kidney
damage. Circulatory failure is another possible type of complication.

6. Diagnosis
Laboratory diagnosis can be achieved by assays of blood, urine, or
hair samples using cold-vapor absorption spectroscopy. 48-58 Mercury
has a very short halflife in the blood, but a relatively long half-life in the
body. This property makes blood samples the best modality for
assessing acute poisoning, whereas urine and hair samples reliably
measure chronic exposure. The established reference levels for blood
and urine samples in adults are also used in children because there
are no firmly established background levels for children. The clinician
should note that the threshold for toxicity in children may be lower than
in adults. Acute mercury poisoning is best assessed by assaying
samples of whole blood and not serum. The blood should be collected
in a heparinized container and immediately refrigerated. Levels of 50
pg per liter or greater are toxic in adults; however, blood levels of
mercury do not necessarily correlate with the degree of clinical toxicity.
The normal reference level in an adult is less than 10 gg per liter

7. Treatment
The best overall treatment for mercury poisoning is p{evention.
Continuing public education and enforcement of environmental
regulations regarding the disposal of industrial waste are indispensable
in the control of mercury exposure in the general population.
Pediatricians should remember to obtain an environmental history in
their patients as part of the routine health care maintenance.
Environmental decontamination of spilled elemental mercury should be
undertaken only by trained personnel. Patients should be advised that
vacuum cleaning of elemental mercury worsens the exposure by
further dispersing the mercury vapor. 36 Electronic equipment such as
computers can absorb metallic mercury vapor and repeatedly
contaminate the air while being used. Local health departments are
available to assist with residential decontamination of accidental
mercury spills.

8. Case studty
A 42 year-old man with IgA nephropathy + nephrotic syndrome was admitted in our Institution.
We processed several laboratory tests, including HBV serology tests: HBsAg 0,24 (ε1,00
reactive), Anti-HBs 0,19 (ε10 immune), Anti-HBc 0,18 (ε1,00 reactive). After 5 days, new
laboratory tests were requested with induction dialysis protocol as clinical information: HBsAg
1,12 (ε1,00 reactive), AntiHBs 0,05 (ε 10 immune), Anti-HBc 0,19 (ε1,00 reactive), IgM
AntiHBc 0,16 (ε1,00 reactive), Anti-HBe 1,95 (δ1,00 reactive) HBeAg 0,42 (ε1,00 reactive).
Once we contacted the responsible physician, we acknowledged that vaccination of the patient
happened near 24 h prior sample collection. As transient HBsAg positivity in patients can occur
post recent HBV vaccination, all dialysis procedures of potentially HBV infected patients were
met and we repeated HBV serology 7 days later: HBsAg 0,29 (ε1,00 reactive), Anti-HBs 0,10
(ε10 immune), Anti-HBc 0,17 (ε1,00 reactive). An external confirmatory HBV DNA viral load
was performed with a non-detected result. Conclusions In this case, HBsAg testing was for
screening purposes applying the dialysis induction protocol but in a time of cost-effectiveness
medicine it is fundamental to optimize procedures to prevent HBV antigen testing too soon
after recent HBV vaccination. Follow-up confirmatory testing is fundamental to differentiate true
infection status and limit the consequences of a false positive.

9. Arsenic
PROPERTIES OF ARSENIC (AS) It is a heavy metallic inorganic
irritant poison Inorganic arsenic compounds are poisonous:
Arsenic trioxide, sodium arsenite, arsenic sulphide,
copperarsenite, etc. Metallic arsenic is non poisonous if
ingested because it is not absorbed
MECHANISM OF ACTION Arsenic ion binds with sulphydryl
group (-SH) of enzymes in the liver, lungs, intestinal walls, spleen
It replaces phosphorus in bones where it may remain for years
It also gets deposited in the hairs
SIGNS & SYMPTOMS Arsenic poisoning clinically manifests in
three forms 1. ACUTE FULMINATING TYPE: • Symptoms occur
within half an hour when heavy dose (3-5 gm) is taken • Acts on
sulphhydryl groups of enzymes and capillaries inhibiting cellular
metabolism and causing marked dilation of capillaries and
myocardial failure resulting in shock and death

10. Toxicity types
1. 2.SUB ACUTE TYPE( GASTROENTERITIS TYPE): • When small doses of arsenic are given
at repeated intervals • Resembles case of cholera or food poisoning Arsenic poisoning
Cholera Vomiting precedes purging Purging precedes vomiting Stools are rice
water initially and later turn bloodstained Stools are rice water throughout and passed
as involuntary jet Pain in the throat No pain in the throat Voice remains unaffected
Voice rough & whistling Conjunctiva is inflamed Conjunctiva is normal Vomitus
contains mucus, bile and streaks of blood Vomitus is watery
2.6. 3. CHRONIC TYPE: Presents with a sequence of 5 different set of manifestations
Gastrointestinal: presents with gradual weight loss, malnutrition, fatigue, loss of appetite
Catarrhal changes: presents with running nose, headache, conjunctivitis, bronchial
catarrh Raindrop pigmentation: known to produce milk & roses complexion initially,
followed by patchy brown pigmentation of the skin (especially forehead, neck, shoulders)
3.7. 3. CHRONIC TYPE: It might also show hyperkeratosis of the skin of palms and soles
Mees lines: whitish lines 1-2 mm breadth across the nails of fingers and toes
Arsenical neuritis: polyneuritis, optic neuritis, paresthesias, atrophy of extensors resulting
in wrist and foot drop Diagnosis: urinary As level of > 100 mg/24 hrs. Blood levels are
not reliable

11. 1.TREATMENT Butter and greasy substances act as demulcents
Gastric lavage with warm water or freshly prepared hydrated
ferric oxide solution Hemodialysis is the line of choice in
massive arsenic poisoning BAL is the specific antidote. (3 – 5
mg/kg 4 hourly deep IM for 2 days followed by 2 – 3 mg/kg 6
hourly for 2 days and then every 12 hours for 7 days) DMSA,
Penicillamine can also be used Symptomatic therapy Inj.
Vitamin B1 helps in peripheral neuritis
2.9. POSTMORTEM FINDINGS Stomach: velvety red or
brownish, patchy areas with ulceration. Gastric contents emit
garlicky odor Heart: subendocardial haemorrhage Other
viscera: fatty degeneration of liver, kidney & heart Brain may
show inflammation with haemorrhagic spots

12. Diagnosis
Blood test
Urine test

13. Arsenic poisoning and chelation therapy
Food and drinking water are the main sources of arsenic exposure in most
populations. Chronic exposure can result in dermal lesions such as hyperkeratosis and
pigmentation changes, as well as increased risks of skin and other cancer. Chronic
exposure to arsenic dust results in peripheral neuropathy and peripheral vascular
disease and lung cancer [39,40,67,84–86]. Chelating agents such as DMSA, DMPS,
and penicillamine are commonly used in chronic arsenic toxicity. The concomitant use
of DMSA with long carbon chain analogue such as monocyclohexyl and monoisoamyl
DMSA together showed an improved efficiency at reducing the arsenic load when
compared to DMSA alone [40,67,87]. However, a recent randomized placebo-
controlled clinical study showed satisfactory results in response to the use of DMPS in
chronic arsenic poisoning

14. Lead Poisoning

15. Lead poisoning is a medical condition caused by increased levels of the heavy metal lead the body, and this can interfere with a
variety of body processes and causes toxicity to many organs and tissues
Introduction
Lead (Pb) has been used by humans for at least 7000 years, because it is ubiquitous, easy to extract.
Organolead compounds were widely used as gasoline additives and Inorganic lead compounds are used as pigments in
paints, dyes, and ceramic glazes.

16. Exposure:
Lead-containing paint in older housing and aging water infrastructure are primary sources of lead exposure in the general
population and in children.
A major route of exposure for the general population is from food and water.
Airborne lead is a minor component of exposure. Lead absorption by the lungs depends on the form of vapor or/ and particle

17. • Acute poisoning:- In acute poisoning, typical neurological signs are pain, muscle weakness.
Gastrointestinal problems, such as diarrhea, poor appetite, or weight loss.
Absorption of large amounts of lead over a short time can cause shock, Hemolysis
• Chronic poisoning :- usually presents with symptoms affecting multiple systems, but is associated with three main types of symptoms: gastroin
Signs of chronic exposure include loss of short-term memory, depression, nausea, abdominal pain and loss of coordination

18. Pathophysiology of Lead Toxicity
Gastrointestinal and inhalation absorption of lead is the most common route of absorption of lead particles
Adults absorb 5% to 15% of ingested lead and usually retain less than 5% of what is absorbed. Children absorb 40%
to 50% of ingested lead with 32% retention.
The half-life of lead in the blood is about 30 day.
The major route of excretion of absorbed lead is the kidney.

19. Effects of Lead Toxicity
1- Renal System
Kidney remains a vital organ of target upon cumulative exposure to lead may cause acute or chronic nephropathy with several health implicatio
- deficit in tubular transport mechanism
-degenerative changes in tubular epithelium
- renal dysfunction and hypertension
2- Neurological, Neurobehavioral, and Developmental Effects:
The most severe neurological effect of lead exposure is lead encephalopathy
lead blocks calcium entry into the neuron, the neuron releases less neurotransmitter and sends a weaker signal to the next neuron

20. Effects of Lead Toxicity
3- Bone effects:
Bones remain the primary site for storage of lead in the human body after exposure
lead plays as a risk factor for osteoporosis and as an agent that may compromise skeletal development and fracture healing
4- Reproductive system effects:
Lead crosses placenta —> abortion, stillbirth, neuro-developmental problems.
Lead —> decrease sperm count, increase number of abnormal sperms.

21. Signs & symptoms:
GIT : Nausea, vomiting, constipation, blue line
Other: anemia, renal failure gouty arthritis, myocarditis
CNS: Headache, irritability, encephalopathy especially in children.
Diagnosis:
Blood level & Erythrocyte Protoporphyrin: Blood levels more than 30 micro/dL and Erythrocyte protoporphrin level more than 50micro/dL
X-ray on long bone it reveal lead lines.

22. Prevention & treatment:
Prevention:
The phasing out of leaded gasoline and the removal of lead from paint, solder, and water supply pipes have significantly lowered blood lead lev
Decrease exposure by wearing masks and gloves...etc.
Treatment:
Chelation therapy drugs: EDTA, DMSA.
Symptomatic treatment: IV fluids for dehydration, Ca gluconate for lead colic, mannitol to decrease ICT.

23. Environmental CO poisoning

24. Introduction:
Poisoning caused by exposure to toxic levels of carbon monoxide(CO).
CO is a colorless, odorless, and tasteless gas derived from incomplete burning of carbon-containing organic materials.
Undetected, unsuspected, or undiagnosed, carbon monoxide poisoning can result in death.
The most common sources of carbon monoxide include motor vehicle exhaust, smoke from fires, portable kerosene heaters and tobacco smok

25. Pathophysiology
Effects of Carbon Monoxide
CO binds more readily to hemoglobin (Hgb) displacing oxygen and forming carboxyhemoglobin
Premature release of O2 prior to reaching distal tissue leads to hypoxia at the cellular level
Inflammatory response is initiated due to poor and inadequate tissue perfusion
Myocardial depression from CO exposure
• Dysrhythmias, myocardial ischemia, MI
Vasodilation – from increased release of nitric oxide; worsening tissue perfusion and leading to syncope
The major one is the displacement of O2 from hemoglobin, the O2 carrier protein, forming carboxyhemglobin.
CO can also bind to myoglobin

26. Chronic toxicity: It is uncommon because CO does not accumulate. However, repeated exposure cause accumulation of damage e.g. highe
Acute Poisoning
1- Central Nervous System and Heart are most effected.
2- Headache, nausea and fatigue can mimic influenza and food poisoning.
3- Tachycardia

27. Sign & symptoms:
The most common symptoms are headache, dizziness, nausea, and fatigue.
More severe symptoms include loss of consciousness, shortness of breath, confusion, and loss of muscle control.
Diagnosis:
Presence of symptoms consistent with CO poisoning.
an elevated level of carboxyhemoglobin (HbCO). Either arterial or venous blood can be used for testing.

28. Treatment:
The most critical therapy for carbon monoxide poisoning is to start inhaling 100 percent oxygen as soon as possible.

29. Case study
e that she ingested an unknown number of ferrous sulfate tablets. Her initial vital signs were: temperature: 35.4O C; heart rate: 153 bea
Which is the best intervention ?!
- Gastric lavage .
- - Deferroxamine

30. References
1- Toxicology: The Basic Science of Poisons, 9th ed.
2- Schwartz, M. E., & Dhanani, S. (2020). Carbon monoxide poisoning. Salem Press Encyclopedia of Science.
3- Olson, K. (1984). Carbon monoxide poisoning: Mechanisms, presentation, and controversies in management. The Journal Of
Emergency Medicine, 1(3), 233-243. doi:10.1016/0736-4679(84)90078- 7