Virtual Pediatric Patients
Donna M. D'Alessandro M.D., Tamra E. Takle M2
Peer Review Status: Internally Peer Reviewed
The Problem / Clinical Presentation
"Bobby has had a long history of bowel problems. About 2-1/2 years ago, we noticed that he was constipated a lot. He'd have regular movements, then an hour later runny stools or nothing at all for days. We took him to his pediatrician and checked all sorts of things. They tried to give him different medicines, and they tried some behavior therapy, but nothing seemed to help. Then we took him to a specialist about a year ago. Bobby had to go to the hospital a few times to clean him out when he got all plugged up. About a week ago, he was really plugged up and his pediatrician took an x-ray. After the x-ray the doctor asked us questions about the house and if Bobby ever ate things he shouldn't. My wife mentioned that she'd seen Bobby peeling paint and wallpaper off the walls over the last year but she never saw him put it in his mouth. The doctor did some tests and sent us to the University of Iowa because they were abnormal."
Clinical Physical Exam
Bobby was somewhat pale but in no acute distress. His vital signs were normal and stable. He had a height of 109 cm (30th percentile) and weight of 18.2 kg (50th percentile). HEENT was unremarkable. Cardiovascular exam showed a regular rate and rhythm with a Grade I/VI systolic ejection murmur consistent with a flow murmur. Lungs were clear to auscultation bilaterally. The abdomen was soft and nontender and slightly distended with stool palpable in the left lower quadrant. Genitourinary examination was normal with a rectal exam showing decreased tone and a large rectal vault filled with lots of soft stool. Several small bruises were on the skin. Neurologic examination showed normal deep tendon reflexes throughout with normal tone sensation, and ability to tip toe, heel walk and squat.
Clinical Differential Diagnosis
The differential diagnosis for a 5 year old with constipation would include:
His CBC showed Hb=7.7 g/dl, Hct=33%, platelet count=390 K/mm3, WBC=6.8 K/mm3, MCV=64 cu u. Urinalysis was clear. His electrolytes were Na=138 mEq/l, K=4.2 mEq/l, Cl=101 mEq/l, CO2=20 mEq/l, BUN=14 mg/dl , Creatinine=0.4 mg/dl (all are normal). A general screen was normal except serum iron=14 mg/dl (low), TIBC=552 (high), Fe saturation = 3% (low). A peripheral blood smear was done to look for basophilic stippling of erythrocytes, which was not visualized. His lead level was 96 ug/dl.
Laboratory Differential Diagnosis
Plumbism with secondary constipation and iron deficiency anemia
Radiopaque densities were noted in the colon. Dense transverse metaphyseal bands were noted on plain radiographs of the wrist.
Imaging Differential Diagnosis
Dense transverse metaphyseal bands are most commonly seen in lead poisoning. They can also be a normal finding in children 2-6 years old.
No operative intervention was performed
Treatment Course, Prognosis and Follow-up
Since Bobby had a lead level of >70 ug/dl, he was admitted for inpatient chelation therapy with Dimercaprol (BAL) and calcium EDTA. He also received Go-LYTELY for bowel evacuation of lead in his stool.
"We were really surprised when the doctors said Bobby had a high lead level. Thinking back, I remember noticing some white flakes once when he had a bowel movement, but I thought it was maybe left over from a barium test he had one time. My wife even had the paint upstairs tested for lead before, and it was okay. The state medical health department ran some new tests on our house, our water and the soil around the house. My daughters had their lead levels tested too, we're waiting on all the results."
"The doctors mentioned that lead could cause some behavior changes. Bobby's in preschool, and he's been doing pretty well until a few months ago, when his teachers mentioned some increased grumpiness and temper problems and that he's been kind of irritable."
"They said he had a lot of lead in him and they started therapy to get the lead out. They gave him some medicine to clean out his bowels since there were still paint chips you could see on the x-ray. Then he got another medicine to get it out of his blood and his bones. We can't go back to our home until we get the results of the Health Department's tests, and Bobby probably will still need to take medicine at home. The doctors told us when he finished his treatment and the lead is gone, he'll be okay."
Ingestions can be accidental or intentional. The natural curiosity of young children often will lead to ingestions of inert or noxious materials and substances (e.g. such as paper, small toys, medications, etc.). Inadvertent ingestion of appropriate medications also occurs by taking of the wrong amount or too frequent dosing of a prescribed medication. Intentional ingestion occurs because of a suicide attempt or gesture, Munchausen Syndrome, or Munchausen Syndrome by proxy.
Ingestions may be acute or chronic. In general, acute ingestions may be more life threatening, while chronic ingestion carry more morbidity. A chronic ingestion may be life threatening and acute ingestions may carry lifelong morbidities depending on the toxin ingested.
The differential diagnosis is extremely extensive and includes many medications, plant materials, and numerous organic and inorganic toxins.
History and Physical
The history of an acute ingestion is often easier to take because the events are recent. The history elicited from the child or family members should include
Unstable patients should also have an emergent history taken while treatment is being administered (mnemonic is AMPLE - Allergies, Medications taken, Past medical history, Last meal, Events).
Histories concerning chronic ingestions are often more difficult to obtain. The toxin may not be recognized as a noxious substance or the amount taken regarded as trivial and not important to mention to the health care provider. The ingestion may also not be seen by a caretaker or it may be due to occupational or recreational exposure (e.g. Mercury poisoning in the making of hats or by exposure in a laboratory, or lead exposure in glass making).
A complete physical examination is also important, with attention to subtle changes in vital signs, eyes, and skin, and odors from the patient. The specific physical signs seen on the physical examination will be different depending on the toxin ingested. The cardiovascular and neurologic status should receive the highest priority in evaluation.
Laboratory evaluation of an acute ingestion coincides with obtaining the history and physical and treatment of the patient. Samples of body fluids should be obtained including blood and urine toxicology screenings, as well as gastric lavage samples if appropriate. Samples of plants, insects or other materials may be sent to the appropriate laboratory or professional for identification. Radiographs may be helpful if a radiopaque toxin is suspected. Toxin identification accuracy is improved when clinical information is submitted along with the samples.
Chronic ingestion testing for potential toxins suggested by a careful history and physical examination should be undertaken as is appropriate (e.g. Lead testing in a 9 month old who has lead based paint in the living environment).
Other considerations in laboratory testing can include:
Management of acute and chronic ingestions includes five principles:
Removal from continued exposure can be easy (e.g. remove patient from carbon monoxide infiltrated room) or difficult (e.g. find the lead source in a patient whose home has tested negative).
The patient should be stabilized using the "ABC" management strategy for all emergently treated patients even if it is a chronic ingestion.
Enhancing the excretion or removal of the toxin from the patient depends on the toxin and the patient's condition. These strategies may include inducing emesis or diarrhea, use of activated charcoal to absorb the toxin in the gastrointestinal tract and bloodstream, acidification/alkalinization of the urine, diuresis, and dialysis or hemoperfusion.
Relatively few toxins have specific antidotes when one considers the number of potential toxins. These antidotes may have toxic side effects themselves so they need to be used appropriately.
Safety and prevention strategies should be stressed, such as keeping medications in resistant packaging, locked up and away from children, keeping smaller amounts of medication available in the home, choosing non-poisonous plants for landscaping, routine home maintenance such as having the furnace inspected and use of carbon monoxide detectors in the home, and most importantly, routine education about potential problems for families during well child visits.
A complete history including specific lead exposure is key to the diagnosis. The physical exam is rarely helpful. Many children with elevated lead levels are asymptomatic. Vague, nonspecific symptoms may include myalgia, fatigue, irritability, lethargy, abdominal discomfort, decreased concentration, headache, tremor, vomiting or weight loss.
Almost all U.S. children are at risk for lead poisoning. Lead can be toxic to children for several reasons. Lead can enter the CNS more easily in children than adults because the blood-brain barrier is not well-developed. Lead has a higher bioavailability in children than in adults. In addition, childhood behaviors like repetitive hand-to-mouth activity and pica predispose the child to ingestion.
Lead is absorbed through the GI tract and the lungs. The most common source of lead poisoning in children is through lead-based paint, which is frequently found in older and many inner-city homes. Lead tastes sweet, which is why children start and continue to put it in their mouths. Other sources of lead include contaminated soil and dust, tap water, occupational or recreational exposure, airborne lead, and imported or improperly stored food.
Lead interferes with the incorporation of iron into the heme molecule, causing a microcytic, hypochromic anemia with basophilic stippling. Children with lead poisoning are prone to neurotoxicity, although the mechanism is not well understood. Peripheral neuropathy, renal failure and gastrointestinal problems in adults are all associated with lead intoxication.
A CBC should be obtained along with a peripheral smear to evaluate anemia and basophilic stippling. BUN, creatinine and urinalysis are helpful in assessing renal damage. Serum ferritin, TIBC and Fe saturation should also be considered to check for iron deficiency.
Abdominal radiographs can identify lead particles in the gut, a sign of acute lead ingestion. Radiographs of long bones may show lines of increased density at the metaphyseal plate as a result of growth arrest, due to chronic lead ingestion.
All cases of lead poisoning must be reported to the local health department. An inspection of the home and surroundings will follow with decontamination as indicated. Family members should be screened and counseled on how to decrease lead exposure. Chelation therapy is indicated and may be done inpatient with Dimercaprol and/or calcium EDTA for levels >45 ug/dl or outpatient with Succimer (DMSA). If the child's level is between 10-45 ug/dl, parental education, environmental investigation and treatment of iron deficiency anemia is indicated. At these levels, effectiveness of chelation is questionable. After the initial therapy, blood lead levels should be closely monitored. Depending on the duration of exposure, more than one round of chelation therapy may be necessary. Regular follow-up screening is mandatory.
The prognosis for a child with lead intoxication depends on his/her lead level and duration of exposure. The overall effects are difficult to determine for an individual child since the effects on the central nervous system may not show up for years.
Berkowitz, Carol D, Pediatrics A Primary Care Approach. W.B. Saunders and Co. Philadelphia, PA, 1996. pp. 349-353.
Chao J, Kikano GE. Lead Poisoning in Children. American Family Physician 1993: 47(1), 113-121.
Cotran RS, Kumar V, Robbins SL. Robbins Pathologic Basis of Disease 5th Edition. Philadelphia: W.B. Saunders, 1994.
Fleisher, Gary R., Ludwig Stephen, Synopsis of Pediatric Emergency
Medicine. Williams and Wilkins, Baltimore, MD, 1996, pp. 405-446.
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