With progressive deficits related to the posterior fossa (cerebellum and brain stem), a space-occupying lesion such as a tumor (medulloblastoma, ependymoma, brain-stem glioma) should be immediately excluded.
Because of the presence of bone in the posterior fossa, a magnetic resonance imaging (MRI) scan is more sensitive than a computed tomography (CT) scan.
Because of the progressive rather than acute nature, an electroencephalogram (EEG) or drug screen would be less likely to be diagnostic, although it might be considered in an acute process.
Aminoacidurias, detected by an amino acid screen , tend to present at an earlier age.
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Munchausen syndrome occurs in those who purposefully make themselves sick in order to be admitted to the hospital. Injection of insulin to produce hypoglycemia that mimics an insulinoma is one example of this syndrome.
Because C peptide is the internal marker of endogenous insulin release, a patient with an insulinoma (benign tumor of islet cells) would be expected to
have a high C peptide,
high serum insulin,
and low serum glucose.
If the C peptide is low, the patient must be taking insulin, because exogenous insulin would lower the patient's own insulin production, therefore lowering the C peptide.
A glucagonoma or a somatostatinoma would be associated with hypoglycemia.
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The findings suggest that the patient has systemic lupus erythematosus (SLE)[READ THE PATHOLOGY OF IT ON MY PATHOLOGY WEBSITE].
The serum antinuclear antibody (ANA) test is the gold-standard screening test to rule out SLE and other collagen vascular diseases.
The major groups of ANA are antibodies against DNA (both double- and single-stranded), histones and nonhistone proteins, and nucleolar antigens.
The ANA provides a titer of the antibody as well as a pattern on immunofluorescence.
The patterns include diffuse (homogeneous), speckled, rim (peripheral), and nucleolar.
Some patterns are specific for certain diseases.
For example, a rim pattern is usually associated with anti-double-stranded (ds) DNA, which is very specific for SLE with renal involvement.
A nucleolar pattern is specific for progressive systemic sclerosis.
The two most specific antibodies (least number of false-positives) for SLE are anti-ds DNA (98%) and anti-Sm (Smith) [100%].
Anti-SSA (Ro) and anti-SSB (La) are positive in Sjögren's syndrome in 70% to 95% and 60% to 90%, respectively.
The presence of anti-SSA (Ro) in a pregnant woman with SLE has a high association with complete heart block in newborns.
Anticentromere antibodies are present in 90% of patients with the CREST syndrome, and antiribonucleoproteins are seen in more than 95% of patients with mixed connective tissue disease.
Antimitochondrial antibodies are noted in more than 90% of cases of primary biliary cirrhosis, and antihistone antibodies are present in more than 95% of patients with drug-induced SLE (most commonly due to procainamide)
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A 47-year-old homeless male alcoholic presents with a fever and expectoration of foul-smelling sputum. His dental hygiene is poor. A chest x-ray reveals a cavitary lesion with a fluid layer in the superior segment of the right lower lobe. A Gram's stain of sputum would be expected to show which of the following
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The patient has a lung abscess that is due to aspiration of infected material from the oropharynx.
This condition occurs in patients who are unconscious or obtunded from alcohol.
Poor dental hygiene is invariably present.
Gram's stain classically shows a mixture of aerobic and variable-staining anaerobic organisms, consisting of gram-positive cocci and a mixture of gram-positive and gram-negative rods with tapered ends.
Common anaerobes include
Bacteroides melaninogenicus (faint gram-negative rods),
anaerobic streptococci (small gram-positive cocci),
and Fusobacterium nucleatum (gram-negative rods with tapered ends).
The basilar segments of the right lower lobe are the classic location for aspiration in the upright or sitting position.
The posterior segment of the upper lobe is involved if aspiration occurs when the patient is lying on the right side.
The superior segment of the lower lobe is involved if the patient aspirates in the supine position.
Penicillin plus vigorous bronchial toilet is usually effective in the treatment of anaerobic lung abscesses.
Surgery is rarely indicated.
Gram-positive diplococci in the sputum are most commonly Streptococcus pneumoniae, the most common community-acquired pneumonia.
Fat gram-negative rods with capsules are usually Klebsiella pneumoniae, which is commonly associated with alcoholism.
The abscesses are usually located within areas of lobar consolidation.
Gram-positive filamentous and branching bacteria in the sputum could be Actinomyces or Nocardia.
Actinomyces is a strict anaerobe and is present within sulfur granules.
It produces pleuropulmonary disease, with sinus tracts draining pus out to the skin.
Nocardia is a strict aerobe and is partially acid-fast.
Primary pulmonary disease with abscess formation is most commonly seen in immunocompromised hosts, particularly heart transplant patients.
Gram-positive rods (e.g., Listeria, Clostridium species, Bacillus species) are not common causes of lung abscesses.
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acute lead toxicity, which can present as
wristdrop in an adult
or as encephalopathy in a child.
A nerve conduction velocity (NCV) study would only confirm the clinical diagnosis, not give the cause.
X-rays and magnetic resonance imaging (MRI) scans would give uninformative structural information.
Diabetes is the most common cause of neuropathy, but it would be very unlikely to present initially as a motor neuropathy, because it usually affects sensory fibers clinically first.
Young children have a great potential for lead exposure
are especially susceptible to its toxic effects.
Since blood lead readily crosses the placenta, lead poses a substantial threat to the developing fetus.
Workers may bring lead dust home on skin and clothes and unknowingly expose family members.
Hyperactivity - it's not always ADD
Little Pika appears to have a normal exam. What clues in the history might help establish the presence of lead toxicity?
Answer: The usual symptoms of childhood lead poisoning (in the absence of an encephalopathy) are generally non-specific.
Ask about abdominal colic, behavior-attention disorders, or unexplained retardation-developmental delays
The incomplete development of the blood-brain barrier in very young children (up to 36 months of age) increases the risk of lead's entry into the developing nervous system, which can result in prolonged neurobehavioral disorders.
Children absorb and retain more lead in proportion to their weight than do adults.
Young children also show a greater prevalence of iron deficiency, a condition that can increase gastrointestinal absorption of lead.
Exposure Pathways
Lead is a naturally occurring element that has been used almost since the beginning of civilization.
Because of the many industrial activities that have brought about its wide distribution, lead is ubiquitous in the environment today.
All humans have lead in their bodies, primarily as a result of exposure to manmade sources.
The primary sources of environmental exposure to lead are
leaded paint,
auto emissions,
and drinking water.
Today, the major environmental sources of metallic lead and its salts are paint, auto exhaust, food, and water.
For children, the most important pathways are
ingestion of chips from lead-painted surfaces,
inhalation of lead from automobile emissions,
food from lead-soldered cans, drinking water from lead-soldered plumbing,
and medications in the form of folk remedies.
A wide variety of workers, hobbyists, and substance abusers may
encounter potentially high levels of lead.
Certain folk remedies may also cause lead poisoning.
Automobile emissions have been an important source of lead exposure for urban residents, particularly in areas with congested traffic.
Although inhalation of lead from gasoline is no longer considered a public health problem, the lead from dust in automobile emissions has been deposited in the soil.
Children playing near roads and freeways may come in contact with contaminated soil.
Lead enters the body primarily through ingestion and inhalation.
Sources of lead exposure
Occupational
Plumbers, pipe fitters
Lead miners
Auto repairers
Glass manufacturers
Shipbuilders
Printers
Plastic manufacturers
Lead smelters and refiners
Police officers
Steel welders or cutters
Construction workers
Rubber product manufacturers Gas station attendants
Battery manufacturers
Bridge reconstruction workers
Firing range instructors
Environmental
Lead-containing paint
Soil/dust near lead industries, roadways, lead-painted homes
Plumbing leachate
Ceramicware
Leaded gasoline
H obbies and Related Activities
Glazed pottery making
Target shooting at firing ranges
Lead soldering (e.g., electronics)
Painting
Preparing lead shot, fishing sinkers
Stained-glass making
Car or boat repair
Home remodeling
Substance Use
Folk remedies
"Health foods"
Cosmetics
Moonshine whiskey
Gasoline "huffing"
Biologic Fate
Once in the bloodstream, lead is primarily distributed among three compartments -- blood, soft tissue, and mineralizing tissue.
The bones and teeth of adults contain more than 95% of total lead in the body.
In times of stress, the body can mobilize lead stores, thereby increasing the level of lead in the blood.
The body accumulates lead over a lifetime and normally releases
it very slowly.
In the human body, inorganic lead is not metabolized but is directly absorbed, distributed, and excreted.
The rate at which lead is absorbed depends on its chemical and physical form and on the physiologic characteristics of the exposed person (e.g., nutritional status and age).
Inhaled lead deposited in the lower respiratory tract is completely absorbed.
The amount of lead absorbed from the GI tract of adults is typically 10% to 15% of the ingested quantity; for pregnant women and children, the amount absorbed can increase to as much as 50%.
The quantity absorbed increases significantly under fasting conditions and with iron or calcium deficiency.
Once in the blood, lead is distributed primarily among three compartments- blood, soft tissue (kidney, bone marrow, liver, and brain), and mineralizing tissue (bones and teeth).
Mineralizing tissue contains about 95% of the total body burden of lead in adults.
The lead in mineralizing tissues accumulates in subcompartments that differ in the rate at which lead is resorbed. In bone, there is both a labile component, which readily exchanges lead with the blood, and an inert pool.
The lead in the inert pool poses a special risk because it is a potential endogenous source of lead.
When the body is under physiologic stress such as pregnancy, lactation, or chronic disease, this normally inert lead can be mobilized, increasing the lead level in blood.
Because of these mobile lead stores, significant drops in a person's blood lead level can take several months or sometimes years, even after complete removal from the source of lead exposure.
Of the lead in the blood, 99% is associated with erythrocytes; the remaining 1% is in the plasma, where it is available for transport to the tissues.
The blood lead not retained is either excreted by the kidneys or through biliary clearance into the gastrointestinal tract. In single- exposure studies with adults, lead has a half-life, in blood, of approximately 25 days; in soft tissue, about 40 days; and in the nonlabile portion of bone, more than 25 years.
Consequently, after a single exposure a person's blood lead level may begin to return to normal; the total body burden, however, may still be elevated.
For lead poisoning to develop, major acute exposures to lead need not occur.
The body accumulates this metal over a lifetime and releases it slowly, so even small doses, over time, can cause lead poisoning.
It is the total body burden of lead that is related to the risk of adverse effects.
Lead affects primarily the peripheral and central nervous systems, the blood cells, and metabolism of vitamin D and calcium.
Lead also causes reproductive toxicity.
Neurologic Effects
The most sensitive target of lead poisoning is the nervous system. In children, neurologic deficits have been documented at exposure levels once thought to cause no harmful effects.
In addition to the lack of a precise threshold, childhood lead toxicity may have permanent effects.
One study showed that damage to the central nervous system (CNS) that occurred as a result of lead exposure at age 2 resulted in
continued deficits in neurologic development,
such as lower IQ scores and
cognitive deficits, at age 5.
In another study that measured total body burden, primary school children with high tooth lead levels but with no known history of lead poisoning had
larger deficits in psychometric intelligence scores,
speech and language processing,
attention,
and classroom performance than children with lower levels of lead. A 1990 follow-up report of children with elevated lead levels in their teeth noted a sevenfold increase in the odds of failure to graduate from high school, lower class standing, greater absenteeism, more reading disabilities, and deficits in vocabulary, fine motor skills, reaction time, and hand-eye coordination 11 years later.
The reported effects are more likely caused by the enduring toxicity of lead than by recent excessive exposures because the blood lead levels found in the young adults were low (less than 10 micrograms per deciliter (mcg/dL)).
Effects in children generally occur
at lower blood lead levels than in adults.
The developing nervous system in children
can be affected adversely at blood lead levels of less than 10 mcg/dL.
Neurologic deficits, as well as other
effects caused by lead poisoning, may be irreversible.
Hearing acuity, particularly at higher frequencies, has been found to decrease with increasing blood lead levels.
Hearing loss may contribute to the apparent learning disabilities or poor classroom behavior exhibited by children with lead intoxication.
Adults also experience CNS effects at relatively low blood lead levels, manifested by
subtle behavioral changes,
fatigue,
and impaired concentration.
Peripheral nervous system damage, primarily motor, is seen mainly in adults.
Peripheral neuropathy with mild slowing of nerve conduction velocity has been reported in asymptomatic lead workers.
Lead neuropathy is believed to be a motor neuron, anterior horn cell disease with peripheral dying-back of the axons.
Frank wrist drop occurs only as a late sign of lead intoxication.
Hematologic Effects
Lead inhibits the body's ability to make hemoglobin by interfering with several enzymatic steps in the heme pathway.
Ferrochelatase, which catalyzes the insertion of iron into protoporphyrin IX, is quite sensitive to lead.
A decrease in the activity of this enzyme results
in an increase of the substrate, erythrocyte protoporphyrin (EP),
in the red blood cells.
Recent data indicate that the EP level, which has been used to screen for lead toxicity in the past, is not sufficiently sensitive at lower levels of blood lead and is therefore not as useful a screening test for lead poisoning as previously thought.
Lead inhibits several enzymes that are critical to the synthesis of heme.
Lead poisoning in children only rarely
results in anemia.
Lead can induce two types of anemia.
Acute high-level lead poisoning has been associated with hemolytic anemia.
In chronic lead poisoning, lead induces anemia by both interfering with erythropoiesis and by diminishing red blood cell survival.
It should be emphasized, however, that anemia is not an early manifestation of lead poisoning and is evident only when the blood lead level is significantly elevated for prolonged periods.
Endocrine Effects
Lead interferes with a hormonal form of vitamin D, which affects multiple processes
in the body, including cell maturation and skeletal growth.
A strong inverse correlation exists between blood lead levels and levels of vitamin D.
Because the vitamin D-endocrine system is responsible in large part for the maintenance of extra- and intra-cellular calcium homeostasis,
it is likely that lead impairs cell growth and maturation and tooth and bone development.
Renal Effects
Lead-induced chronic renal insufficiency may result in gout.
A direct effect on the kidney of long-term lead exposure is nephropathy.
Impairment of proximal tubular function manifests in
aminoaciduria,
glycosuria,
and hyperphosphaturia (a Fanconi-like syndrome).
There is also evidence of an association between lead exposure and hypertension, an effect that may be mediated through renal mechanisms.
Gout may develop as a result of lead- induced hyperuricemia, with selective decreases in the fractional excretion of uric acid before a decline in creatinine clearance.
Renal failure accounts for 10% of deaths in patients with gout.
Reproductive and Developmental Effects
Maternal lead stores readily cross the placenta, placing the fetus at risk.
An increased frequency of miscarriages and stillbirths among women working in the lead trades was reported as early as the turn of the century.
Although the data concerning exposure levels are incomplete, these effects were probably a result of far greater exposures than are currently found in lead industries.
Reliable dose-effect data for reproductive effects in women are still lacking today.
Increasing evidence indicates that lead not only affects the viability of the fetus, but development as well.
Developmental consequences of prenatal exposure to low levels of lead include reduced birth weight and premature birth.
Lead is an animal teratogen; however, most studies in humans have failed to show a relationship between lead levels and congenital malformations.
The effects of lead on the male reproductive system in humans have not been well characterized.
The available data support a tentative conclusion that testicular effects, including reduced sperm counts and motility, may result from chronic exposure to lead.
Carcinogenic Effects
EPA's Science Advisory Board has recommended
that lead be considered a probable human carcinogen.
Case reports have implicated lead as a potential renal carcinogen in humans, but the association remains uncertain.
Soluble salts, such as lead acetate and lead phosphate, have been reported to cause kidney tumors in rats.
Clinical Evaluation
The first signs of lead poisoning in children are often subtle neurobehavioral problems that adversely affect classroom behavior and social interaction.
Speech or hearing impairments, or both, are not uncommon ln lead-exposed children.
The physical examination should include special attention to the
hematologic,
cardiovascular,
gastrointestinal,
and renal systems.
The nervous system, including behavioral changes, should be carefully evaluated.
A purplish line on the gums (lead line) is rarely seen today, but if present, usually indicates severe and prolonged lead poisoning.
For children, hearing, speech, and other developmental milestones should be carefully evaluated and documented. In certain geographic areas, iron deficiency is common in children 9 to 24 months of age.
Since iron and calcium deficiencies are known to enhance the absorption of lead and to aggravate pica, it is especially important to assess the nutritional status of young children.
Signs and Symptoms
Most persons with lead toxicity are not overtly symptomatic.
Because of differences in individual susceptibility, symptoms of lead intoxication and their onset may vary.
With increasing exposure, the severity of symptoms can be expected to increase.
Those symptoms most often associated with varying degrees of lead toxicity are listed below. In symptomatic lead intoxication, blood lead levels generally range from 35 to 50 mcg/dL in children and 40 to 60 mcg/dL in adults.
Severe toxicity is frequently found in association with blood lead levels of 70 mcg/dL or more in children and 100 mcg/dL or more in adults.
Continuum of signs and symptoms associated with lead toxicity
Mild Toxicity
Myalgia or paresthesia
Mild fatigue
Irritability
Lethargy
Occasional abdominal discomfort
Moderate Toxicity
Arthralgia
General fatigue
Difficulty concentratingI>Muscular exhaustibility
Tremor
Headache
Diffuse abdominal pain
Vomiting
Weight loss
Constipation
Severe Toxicity
Paresis or paralysis
Encephalopathy-may abruptly lead to seizures, changes in consciousness, coma, and death
Lead line (blue-black) on gingival tissue
Colic (intermittent, severe abdominal cramps)
lead encephalopathy
In the acute presentation, there may be
persistent vomiting,
seizures,
ataxia,
altered mental status,
papilledema and coma.
A spinal tap (carefully performed after CT) might reveal
pleocytosis,
mild elevated protein
and increased opening pressure.
Lead encephalopathy rarely occurs at blood lead levels below 100 µg/dL.
However, children with elevated blood lead levels, even well below 100 µg/dL, may present with a constellation of neurologic symptoms
Some of the hematologic signs of lead poisoning mimic other diseases or conditions.
In the differential diagnosis of microcytic anemia, lead poisoning can usually be ruled out by obtaining a venous blood lead concentration;
if the blood lead level is less than 25 mcg/dL, the anemia usually reflects iron deficiency or hemoglobinopathy.
Two rare diseases, acute intermittent porphyria and coproporphyria, also result in heme abnormalities similar to those of lead poisoning.
Other effects of lead poisoning can be misleading.
Patients exhibiting neurologic signs due to lead poisoning have been treated only for peripheral neuropathy or carpal tunnel syndrome, delaying treatment for lead intoxication.
Failure to correctly diagnose lead induced gastrointestinal distress has led to inappropriate abdominal surgery
Laboratory Evaluation
If pica or accidental ingestion of lead-containing objects (such as curtain weights or fishing sinkers) is suspected, an abdominal radiograph should be taken.
Hair analysis is not usually an appropriate assay for lead toxicity because no correlation has been found between the amount of lead in the hair and the exposure level.
The probability of environmental lead contamination of a laboratory specimen and inconsistent sample preparation make the results of hair analysis difficult to interpret.
Suggested laboratory tests to evaluate lead intoxication include the following:
CBC with peripheral smear
Blood lead level
Erythrocyte protoporphyrin level
BUN and creatinine level
Urinalysis
CBC with Peripheral Smear.
In a lead-poisoned patient, the hematocrit and hemoglobin values may be slightly to moderately low.
The differential and total white count may appear normal.
The peripheral smear may be either normochromic and normocytic or hypochromic and microcytic.
Basophilic stippling is usually seen only in patients who have been significantly poisoned for a prolonged period.
Eosinophilia may appear in patients with lead toxicity but does not show a clear dose-response effect.
Basophilic stippling is not always seen in leadpoisoned patients.
The best screening and diagnostic test for lead poisoning is a blood lead level.
Blood Lead Level.
A blood lead level is the most useful screening and diagnostic test for lead exposure.
A blood lead level reflects lead's dynamic equilibrium between absorption, excretion, and deposition in soft- and hard-tissue compartments.
For chronic exposures, blood lead levels often underrepresent the total body burden; nevertheless,
it is the most widely accepted and commonly used measure of lead exposure. Blood lead levels respond relatively rapidly to abrupt or intermittent changes in lead intake (for example, ingestion of lead paint chips by children) and, within a limited range, bear a linear relationship to those intake levels.
Lead is most harmful to children under 6 years of age.
Every child who has a developmental delay, behavioral disorder, or speech impairment, or who may have been lead-exposed, should be considered for a blood lead test.
Equally important, siblings, housemates, and playmates of children with suspected lead toxicity probably have similar exposures to lead and should be promptly screened.
For occupationally exposed adults, consult the federal lead standard for the mandated type and frequency of lead screening (see Workplace, Air).
Today, the average blood lead level in the U.S. population is below 10 mcg/dL, down from an average of 16 mcg/dL (in the 1970s), the level before the legislated removal of lead from gasoline.
A blood lead level of 10 mcg/dL is about 3 times higher than the average level found in some remote populations.
The levels defining lead poisoning have been progressively declining. (See Biologic Guidelines in Standards and Regulations.) Currently, the consensus level of concern for children is 10 to 14 mcg/dL .
Effects on stature have been reported to begin at levels as low as 4 mcg/dL, the present limit for accurate blood lead measurement.
Taken together, effects occur over a wide range of blood lead concentrations, with no indication of a threshold.
No safe level has yet been found for children.
Even in adults, effects are being discovered at lower and lower levels as more sensitive analyses and measures are developed.
EP and ZPP
Using an EP or ZPP assay to screen children for lead poisoning is not as useful as once thought.
Treatment and Management
All therapeutic chelating agents have potentially adverse side effects and should be used cautiously.
The type of therapy required will normally depend on the patient's blood lead level.
Asymptomatic patients with blood lead levels below 25 mcg/dL
usually require only separation from the source of exposure.
Children with blood lead levels of 45 mcg/dL or greater should be referred for appropriatechelation therapy immediately.
The EDTA challenge test will indicaate the extent
of lead stores in the body. Some practitioners use this test
when deciding whether to institute chelation therapy
for a patient with a blood level between 25 and 44 mcg/dL.
|
Blood Lead Level (µg/dL)
Blood Lead Level (µg/dL)
|
Recommendation(s)
|
0-9
|
No treatment
|
10
|
"Lead poisoning"
|
10-14
|
Environmental analysis
|
15-19
|
Environmental analysis, education
|
20-24
|
Remove from source, bring to medical attention
|
25-54
|
Remove from source, do EDTA test (see below)
|
55-69
|
Remove from source EDTA or DMSA (see below)
|
70 or symptomatic
|
Emergency hospitalization BAL and EDTA (see below)
Return the child to a clean house
|
EDTA = edetate calcium disodium
DMSA = succimer (dimercaptosuccinic acid)
BAL = dimercaprol
Chelation is the key
And what about asymptomatic children with serum lead levels between 45-69?
Answer: Asymptomtic children at this level almost always should be treated. The treatment may consist of EDTA alone - 1,000 mg/m2 /24 hour intravenously, in a 24-hr infusion or in a short (20 to 30 min infusion) for 5 consecutive days. EDTA is best given intravenously. When the intravenous route is not possible, EDTA may be given intramuscularly. Unfortuantely, IM EDTA is extremely painful, and the pain is only partially relieved if the drug is mixed with procaine. EDTA can be administered again, if needed, after a 2-day interval.
An alternative therapy consists of Succimer, also known as DMSA (Chemet). DMSA can be given orally, has minimal side effects, and appears to be an excellent chelator. However, do not use outpatient DMSA unless you are certain that the child's environment is perfectly clean. Give DMSA for 5 days at a dose of 350 mg/m2 every 8 hours for 5 consecutive days, followed by 2 weeks more of therapy at reduced frequency (350 mg/m2 every 12 hr) for a total of 19 days. Additional courses may be given, if necessary, after a 2-week interval. Repeated courses of treatment may be necessary in these children to bring the blood lead into a safe range (<20 µg/dL).
Don't seize this....
What is the treatment for those children who are symptomatic or with levels >70?
Answer: In symptomatic children, regardless of blood lead level, begin treatment in the hospital setting. Children with blood lead levels of 70 µg/dL or more, even if asymptomatic, should also be considered medical emergencies and immediately hospitalized. Give dimercaprol (BAL 75 mg/m2 every 4 hours; total daily dose of 450 mg/m2), followed by edetate calcium disodium (EDTA 1,500 mg/m2 /24 hour by continuous infusion).
Be sure to start with BAL and then initiate the EDTA only 3-4 hours later. EDTA, by binding zinc, will also cause a burst of delta-aminolevulinic acid (a neuro toxin - see question 8.3 2) that can cause seizures. Continue treatment for 5 days, suspending BAL as soon as the blood lead level falls below 60 µg/dL. Repeated courses of treatment may be necessary in these children until the blood lead level returns to a safe range (<20 µg/dL).
Dust busters
Before Mrs. Plumbody leaves to take Pika for the EDTA test, what do you tell her will be necessary for her family's environmental safety?
Answer: Tell Mrs. Plumbody that the most important aspect of therapy is to remove the child from the source of exposure to lead. It will be necessary for the Health Department to analyze the child's house and environment. Removal of the child from the source of contamination must be complete and keep in mind there may be more than one source (babysitter, grandmother's house, etc). Remove the child to a safer home that has been inspected by the Health Department.
While the child's home is being repaired, the child should stay away from it at all times. Repairs, you tell Mrs. Plumbody, should be followed by cleaning with a high-efficiency particle accumulator (HEPA) vacuum cleaner, then the areas washed and scrubbed thoroughly with a high-phosphate detergent several times and vacuumed again.
Pika smiles at you as you are about to leave the room. She hands you her Dixie cup and asks you if you can get her "some more ice to eat
Specific antidotes for lead poisoning should be administered for both acute and chronic lead poisoning.
These are called chelating agents which bind circulating lead in the blood.
These drugs include Calcium EDTA (given by injection), d-penicillamine (given orally) and more recently, Succimer (DSMA), also given orally.
Because these chlating agents, possibly with the exception of Succimer, only bind circulating lead in the blood, repeat courses may be required because lead is released slowly from soft tissues such as the brain back into the systemic circulation
Treatment of Lead Toxicity
Environmental Changes. Avoidance of further lead exposure is the primary mode of treatment.
Dietary Modifications. Patients with iron deficiency have increased absorption of lead; therefore, iron deficiency should be treated. Adequate calcium, zinc, and protein may also reduce lead absorption.
Chelation Therapy
Treatment of acute poisoning consists of one or more chelating agents.
EDTA
This agent binds to lead and is excreted in urine. The usual daily dose is 1,000 mg/m2 for 5 days, preferably administered intravenously. If the agent is given IM, procaine hydrochloride (Novocain) is added for pain control.
The dose may be repeated every 2 to 5 days as needed. Renal tubular necrosis and reversible hepatocellular disease may occur. Adequate hydration and frequent monitoring of urinalyses is necessary.
Succimer ( Chemet) is the only oral agent approved for chelation of lead. Efficacy is comparable to EDTA.
Succimer is given in doses of 10 mg/kg tid for 5 days and then bid for an additional 2 weeks. The adult dose is 500 mg tid for 5 doses, followed by 500 mg bid for 14 days. Repeated courses may be given, with a minimum of 2 weeks between courses. The 100 mg capsules can be mixed with food or fruit drinks.
Succimer has a "rotten egg" sulfur odor. Common side effects include abdominal pain, nausea, vomiting, diarrhea, and elevation of liver enzyme levels.
Dimercaprol binds with lead and is excreted in urine and bile. Unlike EDTA, it chelates lead from the brain. Dimercaprol is commonly combined with EDTA to treat lead encephalopathy; urine is alkalinized during treatment.
Penicillamine ( Cuprimine, Depen) may be given for treatment of lead poisoning, but it is not FDA approved.
Management of Lead Toxicity
|
Blood Lead Level (Fg/dL)
|
Action
|
<30
|
Monitor history and retest as indicated.
|
30 to 40
|
Monitor blood lead levels every 6 mo. All patients with levels >30 Fg/dL should receive a history, physical examination, screening test for iron deficiency, and environmental modification. If iron deficiency is present, iron supplementation is provided.
|
41 to 50
|
Retest blood lead level every 2 mo until two consecutive results are <40 Fg/dL. If the patient is symptomatic, remove from lead exposure.
|
>50
|
Remove patient from lead exposure until blood level is #40 Fg/dL. Consider treatment with EDTA or succimer (Chemet) if the patient is symptomatic. Retest at least every 2 mo.
|
>80
|
Consider treatment with EDTA or succimer. If encephalopathy is present, dimercaprol and EDTA are given.
|
Follow-up Care
Chelation therapy is discontinued when lead levels are less than 25 Fg/dL.
Therapy should be repeated if the level rebounds to within 5 Fg/dL of the pretreatment value.
Children with blood lead levels between 10-24 Fg/dL
after treatment should continue environmental modification and have periodic blood level monitoring. When pretreatment levels are higher than 45 Fg/dL in children and 80 Fg/dL in adults, blood lead levels should be measured immediately after treatment.
Lead levels should be rechecked in all patients within 7-21 days.
After chelation therapy, close monitoring is warranted for at least 1 year or until blood lead levels have dropped below 25 F g/dL in children and 40 F g/dL in adults.
Children are monitored for developmental and hearing problems.
Prevention
Lead-based paint should be covered or removed. If the water system contains lead solder or pipes, only cold water should be used for cooking and drinking; the cold water tap should be allowed to run for several minutes before water is used.
Pottery that is used for food should be lead-free.
Children should play only in areas that are located away from heavy traffic and away from lead contaminated buildings
|