UW intoxication + cases. ONLY PED UW CASES 03-28 (1)

Question 1

UW. A 1-year-old boy is brought to the office for a routine visit. The patient recently transitioned from breast milk to whole milk and enjoys various table foods, including fruits, vegetables, and grains. The family is vegetarian and adds protein to his diet through beans and nut butters. He says 2 words, recently started walking, and often chews on his toys and books. The family lives in a house built in the 1940s that has nochipping paint and has recently been renovated, except for the basement and bedrooms. Height, weight, and head circumference are at the 50th percentile for age. Physical examination is normal. Capillary blood test results are as follows:
Hb 12.5 g/dL; Lead 12 µg/dL (normal <5 µg/dL). Which of the following is the most appropriate next step in management of this patient?

Answer 1

MEASURE VENOUS LEAD

Home < 1978.
In capilary vein incr. lead.

Question 2

Children are typically exposed to lead through inhalation or ingestion of lead particles from their environment.
What age of house?

Answer 2

home built before 1978, especially if there is peeling paint or dust released during renovation.

Other risk factors include lead piping, having a parent who works with batteries or pottery, or having a playmate or sibling with a history of lead poisoning.
Also: pica, immigrant, low social status

Question 3

UW. Lead. If symptomatic, what CP?

Answer 3

Anemia, abdominal pain/constipation, and encephalopathy, cognitive impairment/behavioural changes

Question 4

UW. LEAD. Targeted screening of high-risk populations regardless of symptoms is important as most children with lead toxicity are initially asymptomatic but can have cognitive and behavioral problems that become apparent after school entry.

Question 5

UW. lead. Capillary (fingerstick) blood specimens positive –> why need take venous sample?

Answer 5

Capilary = false-positive results are common due to environmental contamination and improper collection.
Therefore need venous sample. Abnormal >=5 µg/dL.

Question 6

UW. lead. when need Tx?

Answer 6

chelation therapy is not routinely administered for lead levels <45 µg/dL

Question 7

UW. lead. What is adminitered for Tx?

Answer 7

Dimercaptosuccinic acid (succimer) is typically used when lead levels are 45-69 µg/dL.

Dimercaprol (British anti-Lewisite) plus calcium disodium edetate (EDTA) should be administered on an emergency basis for levels ≥70 µg/dL or acute encephalopathy.

Question 8

UW. A 5-year-old boy is brought to the emergency department due to altered mental status. His mom states that he seemed well until an hour ago when he started acting very restless and developed sudden onset of vomiting and diarrhea. The patient has no chronic medical conditions. He has not received age-appropriate vaccinations. Temp. 36.7 C, BP 130/85, pulse 148/min, RR are 30/min. The patient is agitated, uncooperative, and drooling. His airway is widely patent, and his voice is normal. Bilateral wheezing is noted on auscultation of the lungs. The abdomen is soft and nontender with increased bowel sounds. Rectal examination shows loose brown stool. Neurologic examination reveals myoclonus. What is the most likely cause of this patient’s symptoms?

Answer 8

NICOTINE POISONING

Question 9

UW. nicotine intoxication in kids: accidental or intentional exposure to nicotine by ingestion (eg, cigarette ends, concentrated liquid nicotine used in e-cigarettes), inhalation, or transdermal absorption (eg, green tobacco sickness).

Answer 9

.

Question 10

UW. nicotine intoxication. CP in mild?

Answer 10

Mild cases can present with gastrointestinal symptoms only.

Question 11

UW. nicotine intoxication. CP in severe?

Answer 11

Severe ingestions can lead to cardiovascular collapse and death.

Question 12

UW. nicotine intoxication. CP biphasic. early < 1h’; late 1-4h.

Answer 12

.

Question 13

UW. nicotine intoxication. CP biphasic. early < 1h. CP?

Answer 13

Early phase (<1 hr) is the stimulatory phase resulting from the relatively small concentration of nicotine acting as an agonist at the nicotinic receptors. Symptoms include agitation, nausea/vomiting, hypertension, tachycardia, myoclonus, and seizures, which are consistent with sympathetic stimulation.

Question 14

UW. nicotine intoxication. CP biphasic. late 1-4h. CP?

Answer 14

Late phase (~1-4 hr) is the inhibitory phase. Larger concentrations of nicotine overwhelm the nicotinic receptors, resulting in functional inhibition that can manifest as delayed parasympathetic effects (eg, bradycardia, hypotension, coma) and neuromuscular blockade (eg, muscle paralysis, weakness).

Question 15

UW. nicotine intoxication.
Nicotine also commonly produces variable muscarinic effects, including sialorrhea (ie, drooling), wheezing, and diarrhea, as seen in this patient.

Answer 15

.

Question 16

UW. nicotine intoxication. Tx - primary?

Answer 16

is primarily supportive (eg, intravenous fluids, airway management).

Question 17

UW. nicotine intoxication. Tx for seizures?

Answer 17

BZD

Question 18

UW. nicotine intoxication. Tx for bradycardia and muscarinic symptoms?

Answer 18

atropine

Question 19

UW. nicotine intoxication. Tx if transdermal exposure?

Answer 19

decontamination

Question 20

UW. caustic ingestion.

An 18-month-old boy is brought to the emergency department an hour after drinking liquid oven cleaner from an unlocked kitchen cabinet. His parents tried to give him water and milk, but he has difficulty swallowing. The boy also has blood-tinged oral secretions. His vital signs are stable. Examination shows an anxious child who is crying and drooling. His lips and chin are swollen and erythematous. He has no stridor and his breathing pattern appears normal. Lungs are clear to auscultation. His shirt is covered in oven cleaner. Which of the following is the best next step in management of this patient?

Answer 20

CLOTHING REMOVAL (vs upper endoscopy)

Upper gastrointestinal endoscopy (Choice G) is recommended within 24 hours to assess the extent of the injury.

The extent of the injury may not be apparent if performed immediately, and delayed endoscopy increases perforation risk.

Question 21

UW. caustic ingestion. Dont do anything that cause VOMITING!!!

Answer 21

Any intervention that could provoke vomiting should be avoided. This includes administration of milk, water, activated charcoal, vinegar, or nasogastric lavage, as vomiting can increase the extent of injury.

If need to insert nasogastric tube - do it with endoscopy. Blindly insertion can cause perforation.

Question 22

UW. organophosphate.

3y/o boy + being found in a storage shed struggling to breathe. His parents are unsure of what has happened and note that multiple chemicals are stored in the shed. Temp. 36.6 C, BP 98/65, pulse 58/min, RR 40/min. SpO2 86% on room air. On examination, the patient is lethargic; his body and clothes are soiled with vomit. The pupils are pinpoint bilaterally, and there is significant watering of the eyes. Auscultation of the lungs demonstrates widespread rhonchi with prolonged expiration. Muscle fasciculations are noted in the extremities. Following endotracheal intubation, which of the following is the most appropriate next step in management of this patient?

Answer 22

REMOVE CLOTHING AND IRRIGATE THE SKIN (vs administer physostigmine)

Question 23

UW. organophosphate. Tx

Initial management includes patient stabilization (ie, airway, breathing, circulation) and decontamination. This includes removal of exposed clothes, which can be contaminated both from topical chemical exposure and by vomiting/diarrhea after chemical ingestion. This should be followed by copious irrigation of the skin and/or eyes to prevent cutaneous absorption. Health care personnel should use personal protective equipment (ie, gloves, gown) and work in a well-ventilated examination room to prevent accidental exposure.

Answer 23

.

Question 24

UW. organophosphate. To counteract the effects of organophosphate poisoning, what administer?

Answer 24

ATROPINE

Question 25

UW. organophosphate. Tx: atropine followed with what?

Answer 25

followed by pralidoxime

Question 26

UW. organophosphate. Tx with Physostigmine =WRONG. An acetylcholinesterase inhibitor, is sometimes used to treat anticholinergic toxicity, which is characterized by flushing, anhidrosis, hyperthermia, mydriasis, and urinary retention. It would worsen this patient's condition

Answer 26

.

Question 27

UW. 8-year-old boy is brought to the emergency department due to a bee sting. His mother removed the stinger and applied ice last night, but upon waking this morning, she noticed the patient's right hand was swollen and mildly painful. Vitals normal. On the dorsum of his right hand, there is swelling, redness, and induration extending 11 cm from a central clear area. It is painful to make a fist. Perfusion and sensation are intact in his fingers. Which of the following is the most likely cause of this patient's symptoms?

Answer 27

LOCAL LARGE REACTION The exaggerated area (~10 cm) of swelling, induration, and redness on this patient's hand after a sting by a member of the Hymenoptera species (eg, bees, yellow jackets, wasps) is called a large local reaction (LLR).

Question 28

UW. LOCAL LARGE REACTION.Mx?

Answer 28

Cold compresses Ora/topical steroids Antihistamines anti-inflammatory medications

Question 29

UW. LOCAL LARGE REACTION.CP?

Answer 29

~ 10 cm or more localized swelling, erythema, warmth Develop withint 24h, peak within 24-48h; resolves 5-10 d. mediated by IgE

Question 30

UW. LOCAL LARGE REACTION. vs cellulitis?

Answer 30

Cellulitis is characterized by skin findings similar to LLRs (eg, erythema, warmth, tenderness). However, superinfections are uncommon in insect bites and would generally occur 3-5 days after the initial bite, not within the first 24 hours, as in this patient.

Question 31

UW. ITEM 1 of 2. A 15-month-old boy is brought to the emergency department with cyanosis. Over the past week, the patient has been teething and has had mild nasal congestion and low-grade fevers. He has been eating and drinking normally. The patient was extremely fussy today, despite his mother giving him acetaminophen and a topical anesthetic that she used when she had a toothache. He was hospitalized for bronchiolitis 6 months ago but is otherwise healthy, and immunizations are up to date. Blood pressure is 90/60 mm Hg, pulse is 158/min, and respirations are 50/min. Pulse oximetry is 85% on room air. Physical examination shows a sleepy child with blue discoloration of the skin and nails. The lungs are clear to auscultation bilaterally. Cardiac examination reveals no murmurs or gallops. The abdomen is soft, nontender, and has no hepatosplenomegaly. Blood samples, including arterial blood gas on room air, are obtained for laboratory testing. Subsequently, 100% oxygen is administered but fails to increase the pulse oximetry reading or the cyanosis. Which of the following laboratory findings would most likely be seen in this patient?

Answer 31

Normal PaO2 Dx methemoglobinemia (uncommon)

Question 32

Uw. methemoglobinemia table. Hx?

Answer 32

exposure to oxidizin substances (eg dapsone, nitrites, local/topical anesthetic)

Question 33

Uw. methemoglobinemia table. CP?

Answer 33

Cyanosis pulse oxymetry SpO2 ~ 85 proc. Dark chocolate-colored blood Additional clinical features may include lethargy, respiratory depression, seizures, and death

Question 34

Uw. methemoglobinemia table. Labs? 2

Answer 34

Saturation gap (>5 proc,. difference between oxygen saturation on pulse oximetry and ABG) Normal PaO2

Question 35

Uw. methemoglobinemia. In normal hemoglobin, iron is in the ferrous (Fe2+) state. When exposed to an oxidizing agent, at least one of the four iron molecules is oxidized to the ferric (Fe3+) state, resulting in acute methemoglobinemia. Ferric iron is unable to bind oxygen;

Answer 35

The increased oxygen affinity prevents oxygen release in peripheral tissues (ie, decreased oxygen delivery).

Question 36

Uw. methemoglobinemia. Because methemoglobin absorbs light at a different wavelength than hemoglobin, patients have pulse oximetry readings of ~85% regardless of the true oxygen saturation level (as seen in this patient).

Answer 36

.

Question 37

Uw. methemoglobinemia. Is Supp. oxygen effective?

Answer 37

Supplemental oxygen has no effect on the altered methemoglobin structure; therefore, it does not improve cyanosis, blood color, or pulse oximetry readings.

Question 38

Uw. methemoglobinemia. why in ABG normal PaO2?

Answer 38

In contrast, arterial blood gas testing analyzes only unbound arterial oxygen (as opposed to hemoglobin-bound oxygen) and displays a falsely elevated oxygen saturation level, shown as normal PaO2.

Question 39

UW. Item 2 of 2. Which of the following should be administered to this patient (with methemoglobinemia)?

Answer 39

METHYLENE BLUE

Question 40

Uw. methemoglobinemia. mechanism of methylene blue?

Answer 40

Methylene blue acts as an electron acceptor for NADPH and is reduced to leucomethylene blue, which in turn reduces methemoglobin to hemoglobin. High-dose ascorbic acid (vitamin C) acts as a reducing agent and can be used when methylene blue is unavailable or contraindicated (eg, glucose-6-phosphate dehydrogenase deficiency).

Question 41

Uw. methemoglobinemia. antidote?

Answer 41

methylene blue

Question 42

UW. kiti ats. Fomepizole is used for the treatment ?

Answer 42

ethylene glycol or methanol ingestion. inhibition of alcohol dehydrogenase, fomepizole prevents the metabolism of these alcohols to their toxic metabolites.

Question 43

UW. kiti ats. Dimercaprol, a chelating agent, is most commonly used in?

Answer 43

treatment of lead poisoning to increase the urinary and fecal excretion of lead.

Question 44

UW. kiti ats. glucagon in what intoxication?

Answer 44

Glucagon can be used after the ingestion of a beta blocker or calcium channel blocker by activating adenylate cyclase, which increases intracellular calcium and improves cardiac contractility.

Question 45

UW. kiti ats. pralidoxime is antidote for what?

Answer 45

Pralidoxime is an antidote for cholinergic toxicity (eg, acetylcholinesterase inhibitors such as organophosphates). Pralidoxime is given with atropine and reactivates the cholinesterase enzyme.

Question 46

UW. acute iron poisoning. CP?

Answer 46

Abdominal pain,hematemesis Shock Liver necrosis

Question 47

UW. acute iron poisoning. Diagnostics? 3

Answer 47

Anion gap metabolic acidosis Elevated serum iron Radiopaque pills on abdominal xray

Question 48

UW. acute iron poisoning. Tx? 2

Answer 48

First line - aggresive fluids for iron chelating = DEFEROXAMINE Whole bowel irrigation If deferoxamine ineffective = dialysis

Question 49

UW. A 3-year-old boy is brought to the emergency department by his pregnant mother after developing severe abdominal pain within the past hour and having several episodes of vomiting. The patient's vomit is black and red in color. Blood pressure is 80/50 mm Hg, pulse is 140/min, and respirations are 30/min. On physical examination, he is irritable and lethargic. Examination shows a normal oropharynx. Cardiopulmonary examination is normal. The abdomen is soft and mildly tender at the epigastrium; there is no hepatosplenomegaly. The extremities are cool to the touch. Laboratory results are as follows: Complete blood count Hemoglobin 12.5 g/dL Platelets 175,000/mm3 Leukocytes 12,500/mm3 Serum chemistry Sodium 140 mEq/L Potassium 3.7 mEq/L Chloride 104 mEq/L Bicarbonate 18 mEq/L Blood urea nitrogen 10 mg/dL Creatinine 0.4 mg/dL Glucose 100 mg/dL Chest x-ray is normal. Abdominal imaging shows several radiopaque tablets in the stomach. Intravenous normal saline is started. Which of the following is the best next step in management of this patient?

Answer 49

DEFEROXAMINE

Question 50

UW. iron intoxication. Vomitus and stool may appear black or green from disintegrating iron tablets.

Answer 50

Hypovolemia from gastrointestinal losses may lead to shock, a potential complication in this patient with hypotension and tachycardia.

Question 51

UW. iron itoxication. formula for acid gap?

Answer 51

sodium − [chloride + bicarbonate]

Question 52

UW. iron itoxication. first line Tx?

Answer 52

First-line treatment of acute iron poisoning is aggressive volume resuscitation.

Question 53

UW. iron itoxication. excessive iron tx with what?

Answer 53

Excessive iron is treated with deferoxamine, a chelating agent that binds free iron, forming a complex that can be renally excreted.

Question 54

Uw. kiti ats. Calcium gluconate treats what?

Answer 54

hyperkalemia

Question 55

Uw. kiti ats. Hemodialysis removes free circulating iron and may be considered on occasion if deferoxamine fails to improve symptoms of iron poisoning.

Answer 55

.

Question 56

Uw. kiti ats. N-acetylcysteine is used in ...

Answer 56

acetaminophen toxicity

Question 57

Uw. kiti ats. Naloxone reverses ...?

Answer 57

narcotic overdose

Question 58

Uw. kiti ats. Oral succimer can be used as a chelating agent in

Answer 58

lead poisoning

Question 59

Uw. kiti ats. Warfarin (a vitamin K antagonist) toxicity can present with ....?

Answer 59

severe hemorrhage (eg, hematemesis, intracranial bleed) and is treated with exogenous vitamin K (phytonadione). warfarin is not radiopaque.

Question 60

UW. A 4-year-old boy is brought to the emergency department by his father due to nausea, vomiting, diarrhea, and abdominal pain over the past 4 hours. Their home bathroom is being repainted due to peeling paint, and prior to the onset of symptoms the patient's father noticed that several pill bottles were open. Temperature is 37.2 C (99 F), blood pressure is 76/38 mm Hg, pulse is 160/min, and respirations are 34/min. On physical examination, the patient appears tired and is responsive only to painful stimuli. The oropharynx is clear but appears dry. Peripheral pulses are weak, and capillary refill is 4 seconds. Not long after examination, the boy develops hematemesis. Laboratory results are as follows: Complete blood count Hemoglobin 13.5 g/dL Platelets 300,000/mm3 Leukocytes 6,800/mm3 Serum chemistry Sodium 143 mEq/L Potassium 4.8 mEq/L Chloride 102 mEq/L Bicarbonate 14 mEq/L Blood urea nitrogen 31 mg/dL Creatinine 1.1 mg/dL Glucose 118 mg/dL Arterial blood gas pH 7.30 PaO2 90 mm Hg PaCO2 30 mm Hg Chest and abdominal x-rays reveal several small opacities in the stomach and duodenum. Which of the following was most likely ingested by this patient?

Answer 60

IRON

Question 61

UW. Acute iron poisoning classically presents in children age <6 due to unintentional ingestion of prenatal vitamins or concentrated ferrous sulfate tablets.

Answer 61

.

Question 62

UW kiti ats. Acute acetaminophen overdose can cause nausea and vomiting. However, AG metabolic acidosis and gastrointestinal bleeding would not be expected.

Answer 62

.

Question 63

UW kiti ats. Salicylate (eg, aspirin) poisoning presents with ...,.. what specific CP?

Answer 63

nausea, vomiting, and a metabolic acidosis with respiratory compensation. However, tinnitus is a common early sign, and aspirin tablets are not visualized on x-ray.

Question 64

UW kiti ats. Patients with acute lead poisoning have abdominal pain, vomiting, and altered mental status/seizures. Radiopaque tablets on x-ray may be seen; however, lead is not corrosive to gastric mucosa and does not cause hematemesis. In addition, metabolic acidosis would not be seen.

Answer 64

.

Question 65

UW kiti ats. Patients with a narcotic overdose (eg, oxycodone) typically have CP?

Answer 65

central nervous system and respiratory depression

Question 66

UW kiti ats. Warfarin poisoning can present with bleeding secondary to coagulopathy (eg, hematuria, hematemesis, intracranial hemorrhage). Metabolic acidosis does not occur.

Answer 66

.

Question 67

A 5-year-old boy is brought back to the emergency department by his grandmother due to "bizarre behavior" a day after being seen there for a left eye injury sustained while playing flag football. At that time he was diagnosed with traumatic iritis and prescribed cyclopentolate eye drops for symptomatic relief. Two hours ago, he began acting strangely and said there were green men outside his house. Temperature is 37.8 C (100 F), blood pressure is 130/75 mm Hg, pulse is 150/min, and respirations are 24/min. He is agitated and disoriented, and he does not answer questions appropriately. The pupils are 8 mm bilaterally, and visual acuity is decreased. Perilimbal conjunctival injection of the left eye is present. Extraocular movements are intact. Mucous membranes are dry. Heart sounds are regular and rapid without a murmur or rub. The lungs are clear to auscultation. Deep tendon reflexes are normal. Which of the following is the best next step in management of this patient?

Answer 67

physostigmine

Question 68

UW. cyclopentolate eye drops -> anticholinergic toxicity. Tx in severe cases?

Answer 68

Treatment for anticholinergic toxicity begins with supportive care (eg, stabilization of airway, breathing, circulation), and mild cases often resolve with supportive therapy alone. For patients such as this one, with severe toxicity that is both peripheral (eg, dilated pupils, dry mucous membranes) and central (eg, hallucinations), physostigmine is recommended.

Question 69

UW. cyclopentolate eye drops -> anticholinergic toxicity. Physostigmine reversibly inhibits acetylcholinesterase in both the peripheral nervous system and CNS; this increases the concentration of acetylcholine and overcomes the anticholinergic blockade.

Answer 69

.